National Poisoning guideline-BD 2009 - 17.01.09

Contents
Training Manual on
Management of Poisoning Guideline-
2009
National Poison Information Centre
Dhaka Medical College
World Health Organization (WHO)
Training Manual on Management of Poisoning
Guideline- 2009
EDITORS:
Prof. Md. Abul Faiz
Dr. Shakil Ahmed
Dr. Md. Robed Amin
Dr. Aniruddha Ghose
Dr. Md. Mizanul Hoque
STATEMENT OF WHO ENVIRONMENTAL HEALTH UNIT
The WHO Environmental Health Programme supports the Government of Bangladesh and its
associated institutions, as well as civil society, in capacity building for environmental health.
Since 1972 WHO has mainly concentrated its assistance on water supply, sanitation and hygiene
promotion, through the Department of Public Health Engineering.
In recent years, support has focused on the development of water quality surveillance systems,
through provision of support to the four DPHE zonal laboratories, training, pilot projects and
fellowships. The management information system shows clearly that it is imperative to give
more attention to operation and management, and water quality aspects of the growing number
of Pourashava drinking water supply systems. Attention has now turned to promoting the
implementation of water safety plans, which is fundamental to a preventive water management
approach.
The detection of arsenic in groundwater has given rise to a diverse package of support measures
covering analytical, technical and health aspects of arsenic mitigation. Access to safe drinking
water may have fallen to around 80% from 97% coverage due to contamination of drinking
water with arsenic. WHO collaborates with Government and together with other development
partners to remedy this situation.
Access to adequate sanitation has been dramatically increased as a consequence of the
Governments launching of the National Sanitation Campaign and is on track to achieve total
coverage by 2010. In addition to the necessary infrastructure attention must be given to
improving hygiene behavior to ensure that the maximum health impact can be derived from the
progress in sanitation access. The diarrhoeal disease burden remains relatively high and an
integrated approach to ensuring safe drinking- water, sustainable sanitation and hygiene
promotion should continue to be pursued.
During the 1990s the importance of environmental factors on health has become increasingly
clear. The WHO supported Healthy Settings Programme attempts to address the linkages
between health and environment through partnerships between municipal authorities, NGOs and
civil society, using situation analysis for participatory action in issues such as solid waste
management, school health, aspects of primary health care, vector control, and urban
development planning.
Capacity building in other areas of Health and Environment is supported through programmes on
chemical safety and hazardous waste management (hospital waste management), air-pollution
and vector borne disease control. Research is supported to obtain evidence for health risks
associated with environmental pollution or degradation. These programmes are undertaken in
support of the Department of Environment and the Directorate General of Health Services.
Food safety and good practice in the preparation and storage of foodstuffs is supported through
awareness raising, support to the central laboratory of the Institute of Public Health and through
capacity building of sanitary inspectors at the Upazilla level.
Environmental Health Unit
world Health Organization
DPHE Bhaban (4th floor)
14, Shaheed Cap. MonsurAli Sarani Kakrail,
Dhaka 1000, Bangladesh
TRAINING MANUAL ON MANAGEMENT OF POISONING
GUIDELINE- 2009
PUBLICATION DATE:
First Published- November 2007, Dhaka, Bangladesh.
Second edition-
Published by -
Dhaka, Bangladesh
All rights reserved by -

Dhaka, Bangladesh
ISBN: 984 300 00062 6
© Any part of this book can be reproduced only for public and academic interest.
Guideline updated: 2009 by
PREFACE
1st Edition
“Poison has been defined as a substance which when introduced into or absorbed by the living
organism, causes injury or death.”
Poisoning is an important emergency situation. Cases of acute poisoning are due to wide number
of substances, which vary depending on countries and economic condition. Global environment
is changing constantly. Most of these changes are man made which are necessary for their
survival. Population growth leads to increasing demand of food and shelter and results in
deforestation, rapid urbanization and industrialization, which in turn produce environmental
hazards. The Limited availability of cultivating land results in widespread use of insecticides and
fertilizers.
Improper management of these chemicals and poisons, their abuse and faulty disposal of the
wastes create health hazards and attribute to the existing disease burden.
In children, poisoning is mostly accidental and peak incidence is in the second year of life, 85%
of the accidental poisoning in children occurs among the under-five. Though there no
surveillance data in Bangladesh’s hospital statistics suggests 8-10% of total in-patient children
are accidental poisoning cases.
The concept and practical aspects of management of these poisoning cases are rapidly changing
as a result of newer scientific researches all over the world including Bangladesh. The health is
personnel particularly the attending physicians often find it difficult to keep up with these
updated knowledge base skills.
Basic objective of this training module is orientation and updating of knowledge and skill of
doctors in managing common cases of poisoning, which they come across in their workplace
regularly. The areas of interaction were selected by the Delphi technique in absence of hard
evidence. The module is divided into 14 independent learning units of relevance. The
participants facilitated by resource person’s design the units for group reading, presentation and
discussion in 1 and 1/2 hour. The contributors did laudable work in preparing the module,
editing and finally compiling for printing. The module was enriched with valuable inputs
received from multiple sources including a board of medical teachers, and office of the DGHS,
GOB.
This guideline is updated as far as possible with the available literature books and on poisoning
in different countries and to provide the clinician first line help. The publisher & other web
resources related to this book recommend further reading in all aspects of confusion and does
not take the legal responsibility of the treatment provided to a particular patient. Inputs from the
readers will further furnish this book and are welcome.
PREFACE
2nd Edition
LIST OF CONTRIBUTORS
1. Prof. Md. Abul Faiz Chairman
Professor of Medicine Module Committee
Dhaka Medical College. PlC, DMCH.
2. Prof. Md. Akhtaruzzaman (Late) Member
Ex-Professor and Head of the Dept. of

Forensic Medicine, Dhaka Medical College.
3. Prof. Md. Mostaque Rahim (Swapon) Member Secretary
Professor & Head of the Dept. of Forensic Medicine

Dhaka Medical College. Dhaka.
& Programme Manager, BN, PHE, (PlC)
4. Prof. F.M. Siddiqui Member
Professor of Medicine
Dhaka Medical College.
5. Prof. Md. Shah Alam Member
Professor of Psychiatry
Institute of Mental Health and Research, Dhaka.
6. Prof. Md. Abid Hossain Mollah Member
Professor & Head of the Dept. of Paediatrics

Dhaka Medical College.
7. Prof. Md. Rajibul Alam Member
SSMC and Mitford Hospital.
8. Prof. Md. Ridwanur Rahman Member
Begum Khaleda Zia Medical College.
9. Dr. Md. Humayun Kabir Member
Programme Officer
Directorate General of Health Services
Mohakhali, Dhaka.
LIST OF RESOURCE PERSONS in 1st edition
(Participated in workshop for finalization
of the draft module on 30/05/07 held in Dhaka Medical College)
1. Dr. Md. Shahjahan Bishwas Director General of Health Services, GOB
2. Brig. General Sarker M A Matin Director, Dhaka Medical College Hospital
3. Prof. Md. Abul Faiz Principal, Dhaka Medical College
4. Prof. Md. Shahadat Hossain Dhaka Medical College
5. Dr. Andrew Trevett WHO EH Advisor, Bangladesh
6. Prof. M A Kasham Khandaker Dhaka Medical College
7. Prof. Abu Azahar Sir Salimullah Medical College
8. Prof. FM Siddiqui Dhaka Medical College
9. Prof. Md. Shah Alam Faridpur Medical College
10. Prof. Kazi Md. Jahangir Rangpur Medical College
11. Prof. Md. Abid Hossain MoIlah Dhaka Medical College
12. Prof. Md. Rajibul Alam Sir Salimullah Medical College
13. Prof. Md. Ridwanur Rahman Begum Khaleda Zia Medical College
14. Prof. TC Das Sir Salimullah Medical College
15. Prof. H A M Nazmul Ahsan Dhaka Medical College
16. Prof. Mostaque Rahim Swapon Rajshahi Medical College
17. Prof. Kazi Tariqul Islam Rajshahi Medical College
18. Prof. Md. Enamul Karim Faridpur Medical College
19. Dr. Mizanul Haque Associate Professor, Dhaka Medical College
20. Dr. Syed Mohammad Arif Associate Professor, Dhaka Medical College
21. Dr. AKM Aminul Haque Associate Professor, Dhaka Medical College
22. Dr. Faizul Islam Chowdhury Associate Professor, Dhaka Medical College
23. Dr. Md. Mahtabuddin Hassan Associate Professor, Chittagong Medical College
24. Dr. Abdullah Al Mamun Associate Professor, Dhaka Medical College
25. Dr. Shakil Ahmed Assistant Prof., Sylhet MAG Osmani Medical College
26. Dr. Md. Robed Amin Junior Consultant, Hathajari Health Complex, Ctg.
27. Dr. Shyamol Sarkar Junior Consultant, Dhaka Medical College
28. Dr. Rubina Yeasmin Junior Consultant, Dhaka Medical College
29. Dr. Shafiqul Bari Registrar, Dhaka Medical College
30. Dr. Md. Humayun Kabir DGHS
31. Dr. Aniruddha Ghose RMO, Chittagong General Hospital
32. Dr. Ariful Basher Student, Clinical Toxicology New Castle, Australia
LIST OF RESOURCE PERSONS in 2nd edition
(Participated in workshop for finalization
of the draft module on 23/12/08 held in Dhaka Medical College)
Serial Name and designation Address Email
1 Prof Md. Abul Faiz Director General of Health

drmafaiz@gmail.com
Service
2 Brig. General Abdus Shahid Khan Director, Dhaka Medical
College Hospital
3 Prof Q. Deen Mohammad Principal

dmc_principal@yahoo.co

m
4 Prof M A Kasham Khandaker Prof and Head, Medicine
5 Prof Mahmudur Rahman Director, IEDCR and

mrahman@citechco.net
President of Toxicology
Society of Bangladesh,
Dhaka
6 Prof. M A Azhar Prof of Medicine and
Principal, Sir Salimullah
Medical Colllege
7 Prof. M Ekhlasur Rahman Prof and Head Paediatrics
8 Prof. Nurul Afsar Professor Of Paediatrics
Rangpur Medical College
9 Prof. F M Siddiqui Prof Of Medicine

dsiddiqi@aitlbd.net
10 Prof. Md. Shah Alam Prof of Psychiatry
Faridpur Medicalcollege
11 Prof. Md Zakir Hossain Professor and Head Of
Medicine, Rangpur
Medical College
12 Prof. Abid Hossain Mollah Prof and Head, Paediatrics,
Mymensingh Medical
College
13 Prof. Md. Rajibul Alam Professor of Medicine

profrajib@yahoo.com
14 Prof. Md. Ridwanur Rahman Professor of Medicine

ridwanurr@yahoo.com
Begum Khaleda Zia
Medical College
15 Prof. Mostaque Rahim Swapon Professor of Forensic

dr.mostaque@gmail.com
Medicine, Rajshahi
Medical College
16 Prof. H A M Nazmul Ahasan Professor of Medicine
17 Prof. Md. Enamul Karim Professor of Medicine
18 Prof. Kazi Tariqul Islam Professor of Medicine
Rajshahi Medical College
19 Prof. Md. Mahtabuddin Hassan Professor of medicine
Chittagong Medical
College
20 Prof. Mizanul Haque Professor of Forensic
Medicine and Programme
Manager Of Poison
Information Centre
21 Prof SK Akhter Ahmad Prof of Occupation And

anon@bdcom.com
Environment Department
NIPSOM, Dhaka
22 Dr. Abdullah Al Mamun Associate Prof. and Head
Department of Psychiatry
23 Dr. Faizul Islam Chowdhury Assoc. Prof. of Medicine
24 Dr Syed Mohammad Arif Assoc. Prof. of Medicine

drsm_arif@yahoo.com
25 Dr A K M Aminul Hoque Assoc. Prof. of Medicine
26 Dr Shafiqul Bari Assoc. Prof. of Medicine
Sylhet MAG Osmani
Medical College
27 Dr Shakil Ahmed Assist. Prof. of Paediatrics

shakildr@gmail.com
Sir Salimullah Medical
College
28 Dr Tito Mia Assist. Prof. of Medicine
29 Dr Rubina Yesmin Assist. Prof. of Medicine
30 Dr Md. Robed Amin Assist. Prof. of Medicine

robedamin@yahoo.com
31 Dr Aniruddha Ghose Assist. Prof. of Medicine,

anrdghs@yahoo.com
Chittagong Medical
College
32 Dr Abdus Sattar Assist. Prof. of Medicine,
Chittagong Medical
College
33 Dr Abu Ahmed Assist. Prof. of Paediatrics
Rangpur Medicial College
34 Dr Aparna Das Assist. Prof. of Medicine
Rangpur Medical Colllege
35 Dr Belalul Islam Resident Physician

belalcmc@yahoo.com
Comilla Medical College
36 Dr S.A.J.M. Musa DPM (Training Hospital)
DGHS
10
37 Dr Ashrafi Ahmad DPM (IHSM), DGHS
38 Dr Ariful Basher Diploma in Clinical

arifulbasher@yahoo.com
Epidemiology from
Newcastle University,
Australia & MPH
39 Dr ABM Sayeduzzaman Shohag Coordinator, Poisoning

dr.zaman79@yahoo.com
Research
40 Dr Salamat Khondokar National Consultant ER,

khandekars@searo.who.i
WHO
nt
41 Dr Andrew F Trevett Environmental Health

trevetta@whoban.org
Advisor, ER,WHO
42 Dr Kazi AHM Akram Chief of EHA, WHO miroo51@yahoo.com
43 Sumona Shafinaz Injury Prevention specialist
UNICEF
11
Table of Content
Contents Page
Chapter 1  Introduction to poisoning management

13
Chapter 2  Assessment and diagnosis of poisoned patients
26
 Principles of management of poisoned patients
Chapter 3  Organophosphorus Compound Poisoning

36
Chapter 4  Benzodiazepine and Abusive Substances Poisoning

57
Chapter 5  Corrosive Poisoning
67
Chapter 6  Hydrocarbon (Kerosene) Poisoning
75
Chapter 7  Copper Sulphate Poisoning
80
Chapter 8 Aluminium Phosphide
84

Chapter 9  Methanol Poisoning
88
Chapter 10 Dhatura Poisoning

93
Chapter 11  Puffer Fish Poisoning
98
Chapter 12 Poisoning with Household product
104

Chapter 13  Paracetamol poisoning

109
Chapter 14  Approach to Diagnosis and Management of Snakebite

115
Chapter 15  Deliberate self harm poisoning

134
Chapter 16  Travel Related Poisoning/Commuters poisoning
142
Chapter 17 Prevention of poisoning
145

Annexure  First Aid for poisoning patient , GCS, Dose of antidote

152, 164
12
Chapter-1
Introduction to poisoning management
Duration: 01 hour
Lesson: 01
Objectives:
At the end of the session the participant will be able to:

Describe the definition of poisoning

Tell the type and route of exposure

Describe the different effects of poisoning

Tell the different aspect of poisoning at working place, accidental and
childhood poisoning

Describe the meaning of chemical and medical poisoning and also the
common poisoning symptom and sign
Sl
Content Duration Methods Material
no
01 Ice breaking and

05 min. Presentation ,Question
Transparency/Flip
Introduction to the
and answer
chart
session
02 Pretest 10 min. Questionnaires and

Paper, pen, pencil
answers ( MCQ) of all
units
02 Definition ,type and route

10 min. Presentation,
Multimedia,Board,M
of poisoning
discussion,
arker,
Question and answer

Transparency/Flip
chart
03 Effects of poisoning 10 min. Presentation,

Multimedia,Board,M
discussion,
arker,
Question and answer,

Transparency/Flip
Case presentation
chart
04 Working place,
10 min. Presentation,
Multimedia,Board,M
accidental and childhood

discussion,
arker,
poisoning
Transparency/Flip
Case study
chart
05 Chemical poisoning 10 min. Presentation,

Multimedia,Board,M
discussion,
arker,
Question and answer

Transparency/Flip
chart
06 Summarization 05 min. Discussion,

Board, Marker,
Question and answer

Transparency/Flip
chart
07 Session evaluation and

05 min. Question and answer Board, Marker, Flip
giving thanks to the

chart
participants
Introduction of poisoning management:
What is a poison?
A poison is any substance that causes harm if it gets into the body. Harm can be mild (for
example, headache or nausea) or severe (for example, fits or very high fever), and severely
poisoned people may die.
The amount of a chemical substance that gets into the body at one time is called the dose. A
dose that causes poisoning is a poisonous dose or toxic dose. The smallest amount that causes
harm is the threshold dose.
Exposure to a poison:
When people are in contact with a poison they are said to be exposed to it. The effect of
exposure depends partly on how long the contact lasts and how much poison gets into the
body, and partly on how much poison the body can get rid of during this time. Exposure may
happen only once or many times.
Acute exposure is a single contact that lasts for seconds, minutes or hours, or several
exposures over about a day or less.
Chronic exposure is contact that lasts for many days, months or years. It may be continuous
or broken by periods when there is no contact. Exposure that happens only at work, for
example, is not continuous.
Chronic exposure to small amounts of poison may not cause any signs or symptoms of
poisoning at first. It may be many days or months before there is enough chemical inside the
body to cause poisoning.
How poison gets into the body:
The way poison gets into the body is called the route of exposure or the route of absorption.
The amount of poison that gets into the blood during a given time depends on the route.
1) Through the mouth by swallowing (ingestion)
Most poisoning happens this way. Small children often swallow poison accidentally, and
adults who want to poison themselves may swallow poison. If people eat, drink or smoke
after they have been handling poisons, without first washing their hands, they may
accidentally swallow some of the poison. This is a common cause of pesticide poisoning.
When poisons are swallowed they go to the stomach. Some poisons can pass through the gut
walls and into the blood vessels. The longer a poison stays in the gut the more will get into
the blood and the worse the poisoning will be.
2) Through the lungs by breathing into the mouth or nose (inhalation)
Poisons in the form of gas, vapor, dust, fumes, smoke or fine spray droplets may be breathed
into the mouth and nose and go down the air passages into the lungs. Only particles that are
too small to be seen can pass into the lungs. Larger particles are trapped in the mouth, throat
and nose and may be swallowed. A person may breathe in poison when working with a
poisonous substance inside a building without fresh air, or when spraying pesticide without
wearing adequate protection. Oil or gas heaters, cookers, and fires give off poisonous fumes
which may reach dangerous concentrations if the smoke cannot get outside or if the room
does not have a good supply of fresh air. Poison that gets into the lungs passes into the blood
vessels very quickly because the air passages in the lungs have thin walls and a good blood
supply.
3) Through the skin by contact with liquids, sprays or mists
People working with chemicals such as pesticides may be poisoned if the chemical is sprayed
or splashed onto the skin or if they wear clothes soaked with chemical. Some poisons can
pass through the skin. They pass through warm, wet, sweaty skin more quickly than through
cold, dry skin, and they pass through skin damaged by scratches or burns more quickly than
through undamaged skin. It may be possible to wash poison off the skin before a poisonous
dose gets into the body.
4) By injection through the skin
Poisons can be injected through the skin from a syringe, or a pressure gun, or during
tattooing, or by the bite or sting of a poisonous animal, insect, fish or snake. The injection
may go directly into the blood vessels or under the skin into muscle or fatty tissues. Poison
injected into the blood has a very quick effect. Poison injected under the skin or into muscle
has to pass through several layers of tissue before reaching the blood vessels, so it acts more
slowly.
How poison is carried around the body
Once a poison gets into the blood it is carried to the whole body as the blood is pumped round
the body by the heart.
How the body breaks down poison
Some poisons are changed by the body into other chemicals. These are called metabolites,
and may be less poisonous or more poisonous than the original substance. These changes take
place mostly in the liver.
How poison leaves the body
Unchanged poisons or their metabolites usually leave the body in the urine, faeces or sweat,
or in the air that a person breathes out. Some poisons, like DDT, pass into body tissues and
organs where they may stay for a long time.
Effects of poison
The effects of a chemical substance on the body may be described as either local or systemic.
A local effect is limited to the part of the body in contact with the chemical: the skin, the
eyes, the air passages or the gut. Examples of local effects are skin rashes, skin burns, watery
eyes, and irritation of the throat causing coughing. Many poisons cause local effects, but there
are also many poisons that do not.
A systemic effect is a more general effect that occurs when a poison is absorbed into the
body.
Some poisons cause both local effects and systemic effects. If someone has local effects from
exposure to a chemical it is important to check whether they also have signs or symptoms of
systemic poisoning.
Local effects
1) On the skin
Chemicals that damage the skin cause reddening or a rash, pain, swelling, blisters or serious
burns. The burns are like the burns caused by fire.
An irritant chemical causes itching, a burning feeling, or pain when it first touches the skin,
but does not cause burns if washed off straight away. However, if it is in contact with the skin
for a long time, for example when people wear contaminated clothes for several hours, it
might cause burns.
Some irritant chemicals have no effect the first few times they touch the skin, but with
continued contact they cause reddening or a rash. This might happen with repeated use of a
household cleaner.
Sometimes people become sensitive to a chemical after they have used it many times. They
may have no effects at first but after a few weeks or months they get a rash every time they
use it.
A corrosive or caustic chemical very quickly causes painful burns and destroys the skin.
There may be blisters and the skin may turn grey-white or brown.
2) On the eyes
Irritant or corrosive chemicals can cause severe pain if they get into the eyes. They may very
quickly burn the surface of the eye and cause scars or even blindness. The eyes will look red
and watery. The person may not want to open the eyes and bright light will hurt.
3) Inside the gut
Irritant or corrosive chemicals may damage the mouth and throat or the inside of the gut. The
person will have belly pain, vomiting and diarrhoea, and the vomit and faeces may contain
blood. If the throat is burnt it may swell very quickly, so that the person cannot breathe.
4) Inside the air passages and lungs
Some gases and vapors can irritate the nose, throat and upper air passages and cause coughing
and choking. Some gases and vapors damage the lungs in a way that causes pulmonary
oedema. some of the gases that cause lung oedema also irritate the nose, throat and upper air
passages, and make people cough and choke.
Some poisonous gases, such as carbon monoxide, have no effect on the nose and throat.
Poisonous gases that do not cause coughing and choking are very dangerous because people
may not know they are breathing poison. Petroleum distillate liquids, such as kerosene, may
cause lung oedema when swallowed.
5) At injection sites
Irritant poisons that are injected into the skin, such as poisons from insect stings and snake
bites, may cause pain and swelling where they are injected. People who accidentally inject
themselves with veterinary products, when giving injections to animals or birds, may get local
effects.
6) Systemic effects
There are many ways in which poisons can cause harm:

By damaging organs such as the brain, nerves, heart, liver, lungs, kidneys, or skin. Most
poisons have a greater effect on one or two organs than on other parts of the body. The
organs that are most affected are called the target organs.

By blocking interconnection between nerves.

By blocking energy supply or oxygen supply.
Effects on unborn babies
Some poisons can harm a baby inside the womb. This is most likely during the first three
months of pregnancy when the nervous system and all the major organs begin to form. The
parts of the baby usually affected are the bones, eyes, ears, mouth and brain. If the damage is
very bad the baby will stop growing and die. Some poisonous chemicals may harm a baby in
the womb without harming the mother. This is serious because there is nothing to warn the
mother that her baby is in danger.
When systemic effects happen
Systemic effects only happen when the amount of poison in the body is greater than the
amount the body can get rid of, and the poison builds up and reaches the threshold level.
Some poisonings happen by accident but some happen when people try deliberately to harm
themselves (self-poisoning) or others. There are other circumstances that may result in
poisoning:
- eating food containing poison;
- taking, or being given, the wrong kind of medicine or the wrong dose;
- taking drugs because they change mood or behaviour, or using
- Plants or chemical products for this purpose.
Accidental poisoning
Accidental poisoning may happen when:
- young children or old people handle poisons not knowing what they are;
- people mistake poison for food or drink because it is not in its original container;
- people misuse chemical products or medicines;
- people use or misuse pesticides;
- people work with chemicals;
- People are exposed to carbon monoxide, usually at home.
Poisoning in childhood
Many poisoning accidents in the home happen to small children aged between 1 and 4 years.
At this age children want to explore.
The chemical products most often swallowed by children are:
- household cleaners such as bleach, detergent and disinfectant;
- paraffin and kerosene used as household fuels;
- cosmetics;
- medicines;
- paint and products for household repairs;
- Household pesticides.
Poisoning in old age
Old people may poison themselves accidentally. If they cannot see very well, they may pick
up the wrong bottle and swallow a household cleaner, for example, instead of a drink or a
medicine.
Taking products out of their own containers
Accidents can happen when someone takes a chemical product out of its container and puts it
in another one. The new container does not have the right label so nobody else will know
what is inside. Even the person who did it may forget.
Pesticide poisoning
Most pesticides are also poisonous or harmful to humans if they get on the skin, or if they are
breathed into the lungs in the form of gases, fumes, dust or fine spray droplets, or if they are
swallowed.
Poisoning at work
Many chemicals that are made, used, or stored in workplaces are poisonous. People who work
with these chemicals need to know how to handle them safely to avoid being poisoned.
Sometimes workers may not know that they are handling a poisonous chemical, or they may
know that the chemical is poisonous but not have been told or shown how to handle it safely.
They may not have read the label or the safety information. Sometimes they may know the
dangers but be too lazy or careless to use safe methods. Accidents, fires or explosions at work
may result in chemicals spilling or leaking out of their containers onto roads or into rivers, or
vapors and gases being released into the air. Sometimes chemicals spread over a large area
and poison many people. Chemical waste and empty chemical containers may be serious
safety hazards if they are not dealt with in the right way.
Self-poisoning
People may try to harm themselves by deliberately taking poison -this is called self-poisoning.
In some countries people take medicines to poison themselves, but people living in rural
communities are more likely to take pesticides. People suffering from depression, serious
illness, or alcohol dependence may try to kill themselves by taking poison. They may swallow
large amounts of medicine, pesticide or other poisons.
Poison in food or drink
Food or drink can be contaminated by poison from microscopic organisms such as bacteria,
viruses, or mould, or by chemical poisons. Some plants, mushrooms, animals or sea-creatures
contain poisonous chemicals. Poisons made by plants, animals or microorganisms are called
toxins.
Chemical poisons
There are many ways chemical poisons can get into food and drink, for example:
- when people working with chemicals eat in the workplace or do not wash their hands
before eating;
- when chemicals spill onto food as it is being moved from place to place, or when it is
in a storeroom;
- when food or drink is stored or cooked in containers that are contaminated with
chemicals;
- when people make flour from grain that has been treated with pesticide because it was
meant to be used for seed or bait, not for food;
- when people brew their own alcoholic drinks and produce poisonous alcohols, such as
methanol;
- when water supplies are polluted by accidental spills of chemicals, or by chemical
waste from factories or waste dumps near watercourses.
Abuse of drugs, chemicals or plants
People may take drugs to change their mood or behavior, to feel relaxed, or to get more
energy. This is called drug abuse because it is not a medical use of the drug. Some people
abuse drugs such as heroin, cocaine or barbiturates. Drinking too much alcohol is an
important kind of drug abuse.
Chapter-2
ASSESSMENT, DIAGNOSIS AND PRINCIPLES OF POISONED PATIENT
MANAGEMENT
Duration: 01 hour 30 minutes
Lesson Plan: 02
Objectives:

Assess acutely poisoned patients in respect of consciousness level,
ventilation and circulation

Take History of poisoned patient including circumstantial evidence and
suicide note

Describe the methods of Examination and investigation needed for the
patient

Describe the principles of poisoned patient management
Sl
no
0
Ice breaking and
05 min Presentation, Question
Transparency/Flip chart
1
Introduction to the
and answer
session
0
Assessment of the
15 min Presentation, discussion,
Multimedia, Board,
2
poisoned patients
Question and answer
Marker,
0
Taking History of
15min Presentation, discussion,
Multimedia, Board,
3
poisoned patient
Marker,
Case presentation
0
Methods of
Multimedia, Board,
4
examination
Question and answer Case
Marker,
study
0
Investigation 10 min Presentation, discussion,
Multimedia, Board,
5
Question and answer
Marker,
0
Principles of
Multimedia, Board,
6
poisoning
Question and answer
Marker,
management
Transparency / Flip
chart
0
Summarization 05 min Discussion,
Board, Marker,
7
Question and answer
Transparency / Flip
chart
0
Session evaluation
05 min Question and answer Board, Marker, Flip
7
and giving thanks to
chart
the participants
Introduction:
Assessment:
Airway, Breathing, Circulation and Consciousness, should be assessed in all patients with
poisoning.
Level of consciousness:

The Glasgow Coma Scale (GCS) is commonly used though it is not validated. A
GCS score of less than 8 (not obeying commands, not speaking, not eye
opening) is unarousable unconsciousness.

Are laryngeal (gag) reflexes present? If it is lost, prompt assessment of
respiration is essential.
Airway:
Most common factor contributing to death from poisoning and drug overdose is loss of
airway protective reflex.
Assessment:
o
Patient who are awake and talking- Likely to have intact airway, but should be
monitored closely.
o
In lethargic and obtunded patient- Check gag reflex. If lost: Airway reflex is
likely to be lost.
Breathing:
Along with the airway problem, breathing difficulties are the major cause of morbidity
and mortality in poisoning. These are: ventilatory failure, hypoxia and bronchospasm.
Assessment:
Be done by observing efforts of ventilation, respiratory rate, and cyanosis,
use of accessory muscle of respiration and SP02 by pulse oximetry.
Ineffective respiration and cyanosis are two important clinical parameters
for assessing the ventilation. If these parameters are present, the patient may
need ventilator support.
Pulse oximetry to measure oxygen saturation (Displayed reading is
inaccurate if 02 saturation is below 70%, poor perfusion, presence of
carboxyhaemoglobin and methaemoglobin).

SP02 <90% demands immediate 02 inhalation.

SP02 91-95% states 02 inhalation necessary.

SP02 >95% is normal.
Circulation:
Maintenance of adequate circulation is a must for every case of poisoning and
drug overdose.
Assessment:
Check BP, pulse rate and rhythm, capillary refill time (CRT).
If SBP <90mm Hg and pulse >100/min; patient is in shock.
In Children: SBP <80mm Hg.
In shock CRT >2sec
ECG monitoring may be needed in case of TCA, yellow oleander, Digitalis
glycoside and beta blocker poisoning.
History taking:
Medical, psychiatric, toxicological and socioeconomic history should be taken
in every case of poisoning.
In Adult: 80% of patients who arrived at the hospital are conscious and
diagnosis of self poisoning is made from history. In the rests who are
unconscious, history from relatives, friends or attendants is helpful and
diagnosis is often inferred from brought specimen (e.g. tablet bottles or a
suicide note) or made by exclusion of other causes.
It is pertinent to try to establish the nature of the substance taken, the amount
involved, the route and the time of exposure to anticipate the clinical course and
to assess risks. In children (<13 yrs) history is very unreliable in regard to amount.
Assessment of psychiatric problems:
1
Events that preceded the act
2
Degree of suicidal intent
3
Current problems faced by the patient
4
H/O psychiatric disorder
5
Personality traits and disorder
6
Family and personal history
7
H/O previous self injury
8
Risk of further overdose and subsequent suicide
Circumstantial evidences:

Suicide note is a reliable indicator of drug overdose in absence of evidence
of physical violence as a cause of coma.

Circumstances in which the patient was found: Children may be found
eating potential toxins or with tab around clothing, or having smell of
the ingested substances from body and oral cavity. Similar thing may
be seen in unconscious adults or may be with empty drug containers,
tablets or capsules nearby.
Physical examination:
Initial assessment of vital signs and managed accordingly.
Subsequent examination depends upon type, amount, nature and time of poisoning. Some
common clustering features may point towards a particular poisoning, and are described
below.
10
Common clusters of features that may be diagnostic:
Feature cluster Likely Poison
Coma, hypotonia, hypo-reflexia, plantar

Barbiturates, benzodiazepines and
responses: flexor or non-elicitable,

alcohol combinations, severe
hypotension.
TCA poisoning.
Smell of OPC, bronchorrhea, incontinence

Organophosphorus and carbamate
of urine & stool, miosis and hyper

insecticides, nerve agents
salivation
Coma, miosis, reduced respiratory rate Opioids.
Nausea, vomiting, tinnitus, deafness,

Salicylates
sweating, hyperventilation, vasodilatation,
metabolic acidosis.
Restlessness, agitation, mydriasis, anxiety,

Sympathomimetic drugs
tremor, tachycardia, convulsion,

(Bronchodilator, theophylline)
arrhythmias.
Blindness (usually with other features) Quinine, methanol
Smell of OPC, bronchorrhea, incontinence

Organophosphorus and carbamate
of urine & stool, miosis and hyper

insecticides, nerve agents
salivation
NB: All the features of a particular poison may not be present in a particular case.
Diagnostic trial of antidotes:
Administration of I.V naloxone and flumazenil has been used to make rapid
clinical diagnoses of opioid and benzodiazepine poisoning respectively; this approach
depends on noticeable improvement in the patient's clinical condition within 1-2 minutes.
Toxicological investigations:
Toxicological screening of blood or urine can be used to establish a diagnosis
of poisoning. The concentration is measured in the plasma or serum rather than whole
blood except Carboxyhaemoglobin.
Emergency measurement of plasma concentration of known toxins is necessary for the
following toxins:

Carboxyhaemoglobin

Methanol

Ethanol

Paracetamol

Ethylene glycol

Salicylate

Iron

Theophylline

Lithium

Benzodiazepine
11
12
Screening for unknown toxins:
In multiple drug overdoses benzodiazepine and paracetamol measured routinely.
Laboratory screening for poisons in an unconscious patient usually concentration are
requested when the cause of coma is unknown.
Urine (20ml) is usually a more appropriate fluid for detecting unknown poison. Once
identified their concentration in blood or plasma can be determined by specific method if
necessary.
Non-toxicological investigations:
Inspection of brought specimen - Generic name, amount left in bottle smell color etc.
Inspection of blood:

Chocolate-coloured blood indicates methaemoglobin caused by drugs e.g. Dapsone,
nitrites or nitrates.

Pink plasma suggests hemolytic poisons e.g. sodium chlorate

Brown plasma suggests the presence of circulating myoglobin secondary to
rhabdomyolysis
Inspection of urine:

Brown discolouration of the urine by the presence of heamoglobin (intravascular
haemolysis), myoglobin secondary to rhabdomyolysis or metabolites of paracetamol.

Crystals in primidone overdose or ethylene glycol.
Haematology:
Is of little value except prolongation of prothrombin time in anticoagulants or paracetamol
overdoses and also in snake bite.
Biochemical indicator of various poisoning:

Serum sodium: e.g. hyponatraemia in Ecstasy poisoning.

Serum potassium: e.g. hypokalaemia in theophylline, hyperkalaemia in digoxin
poisoning, rhabdomyolysis and haemolysis.

Plasma creatinine e.g. renal failure in ethylene glycol poisoning.

Blood sugar e.g. hypo or hyperglycaemia in salicylate poisoning.

Serum calcium e.g. hypocalcaemia in ethylene glycol poisoning.

Serum ALT/AST e.g. increased in paracetamol poisoning.

Serum phosphate e.g. hypophosphataemia in severe paracetamol induced renal
tubular damage

RBC cholinesterase activity e.g. organophosphorus and nerve agents poisoning.

Whole blood methaemoglobin concentration e.g. in nitrite poisoning.
Radiology and ECG are of little value but sometimes important for complication
of poisoning. Radiology can be used to confirm ingestion of metallic objects (coins,
button, batteries or ingestion of globules of metallic mercury) and iron tablet.
In ECG sinus tachycardia with prolongation of PR & QRS interval should
prompt consideration of tricyclic antidepressant poisoning. ECG is also important
in yellow oleander poisoning and phenothiazines overdose.
13
Clinical Features and Complications of Poisoning:
The toxicity of a substance and therefore the features of poisoning can generally be
predicted from:

Its physiochemical properties

Its pharmacological / toxicological actions

Its route of exposure

Its dose
These features are classified as either direct or systemic
Principles of Management of Poisoned Patient:
Most patients with self-poisoning require only general care and support of the vital
systems. However, for a few drugs additional therapy is required. The challenge for
clinicians managing poisoned patients is to identify at an early stage, those who are at
risk of developing serious complications and who might potentially benefit from an
antidote or treatment to increase elimination of the poison.
Strategy:

Provide immediate supportive treatment (ABC).

Is the use of an antidote appropriate?

Is it appropriate to attempt to reduce poison absorption?

Is it appropriate to perform toxicological investigations?

Will non-toxicological investigations assist?

Should urine alkalinization, multiple-dose activated charcoal, and
haemodialysis be employed to increase poison elimination?
Airway, Breathing and Circulation (ABC) (See annexure-I)
Respiratory support:
Food, vomit, secretion and dentures should be removed from the patient's mouth and the
pharynx and the tongue prevented from falling back. The patient should be nursed in
left lateral position to minimize the risk of aspiration of gastric contents into the lungs.
If respiratory depression is present, as determined by clinical features and pulse oximetry
or preferably by arterial blood gas analysis. Supplemental oxygen should be
administered in needed. Pulse oximetry alone will detect hypoxia but not hypercapnia.
Loss of the cough or gag reflex is the prime indication for intubation. The gag reflex
can be assessed by positioning the patient on one side and making him or her gag using
a suction tube. In many severely poisoned patients the reflexes are depressed sufficiently
to allow intubation without the use of sedatives or relaxants.
If ventilation remains inadequate after intubation, as shown by hypoxaemia and
hypercapnia, intermittent positive-pressure ventilation (IPPV) should be instituted.
14
Cardiovascular support:
Although hypotension (systolic blood pressure below 90 mmHg) is a recognized feature
of acute poisoning, the classic features of shock - tachycardia and pale cold skin -
are observed only rarely. As a first step the patient should be placed head down position
(the foot end should be elevated by 15 cm). If there is no improvement, infusion of
crystalloid solution should be started. In patients with marked hypotension, volume
expansion with gelatins or etherified starches (e.g. heta- starch, hexa-starch) should be used,
guided by monitoring of central venous pressure (CVP). Urine output (aiming for 35-50
mL/h) is also a useful guide to the adequacy of the circulation.
If a patient fails to respond to the above measures, more intensive therapy is required.
Dobutamine 2.5-10 microgram/kg/min or epinephrine 0.5-2 microgram/kg/min is
indicated in such case. Dopamine 10-20 microgram/kg/min is an alternative (see flow chart).
Arrhythmias are observed occasionally in poisoned patients, for example after the
ingestion of a tricyclic antidepressant or theophylline. All patients with shock should
have ECG monitoring. Known arrhythmogenic factors such as hypoxia,
acidosis and hypokalaemia should be corrected.
IV fluid 20 ml/kg bolus
Crystalloid Solution-Normal Saline
Reassess
(Pulse, BP, Capillary refill)
No improvement Improved BP
Urine passed
Repeat isotonic crystalloid 20ml/kg over 3- Continue fluid,
5 mints And
Correct the cause
Reassess ventilation, Acid-base
balance and electrolytes
No improvement
Improvement
Assess cardiac status (CXR, ECG) Monitor CVP
CVP <10 mmHg

CVP >10 mmHg
CVP >15 mmHg
lonotropic agents, e.g.

Diuretics
Repeat isotonic Crystalloid
or Colloids (5-10 ml/kg)

Dopamine, Dobutamine
Flow chart: - Management in Hypotension/shock
15
16
Care of unconscious patient:
In all cases the patient should be nursed in the lateral position with the lower leg
straight and the upper leg flexed; in this position the risk of aspiration is reduced (see
fig. chapter 17). A clear airway passage should be ensured by removal of any
obstructing object, vomit or dentures, and by backward pressure on the mandible.
Nursing care of the mouth and pressure areas should be instituted.
Immediate catheterization of the bladder in unconscious patients is usually
unnecessary as it can be emptied by gentle suprapubic pressure.
Insertion of a venous cannula is usual, but administration of intravenous fluids
is unnecessary unless the patient has been unconscious for more than 12 hours or
is hypotensive.
On admission, or at an appropriate time post-overdose, a timed blood sample should
be taken. The determination of the concentrations of the drugs will be
valuable in management. Drug screens on blood and urine are occasionally
indicated in severely poisoned patients in whom the cause of coma is unknown.
Some routine investigations are of value in the differential diagnosis of coma or
the detection of poison-induced hypo or hyperkalaemia, hypo or hyperglycaemia,
hepatic and renal failure or of acid-base disturbances. Measurement of
carboxyhaemoglobin, methaemoglobin and cholinesterase activities are of
assistance in the diagnosis and management of cases of poisoning due to carbon
monoxide, methaernoglobin-inducing agents such as nitrites, and organophosphorus
insecticides respectively.
Other Problems:
Body temperature:
Hypothermia - a rectal temperature below 35°C is a recognized complication of poisoning,
especially in older patients or those who are comatose. The patient should be covered
with a 'space blanket' and, if necessary, given intravenous and intragastric fluids at
normal body temperature. Inspired gases should also be warmed to 37°C.
Hyperthermia may develop with CNS stimulant ingestion. Removal of clothing
and sponging with tepid water will promote evaporation.
Rhabdomyolysis:
Rhabdomyolysis can occur from pressure necrosis in drug-induced coma, or as a
complication of sea snake bite or MDMA (Ecstasy) abuse in the absence of
coma. Patients with rhabdomyolysis are at risk of developing firstly, renal failure
from myoglobinaemia, particularly if they are hypovolaemic and have an acidosis,
and. secondly, wrist or ankle drop from the development of a compartment syndrome.
Convulsions:
These may occur in poisoning due to tricyclic antidepressants, mefenamic acid or
opioids. Usually the fits are short-lived but, if they are prolonged, diazepam 10-20 mg
i.v. should be administered. Persistent fits must be controlled rapidly to prevent severe
hypoxia, brain damage and laryngeal trauma. If diazepam in repeated doses is
ineffective, the patient should also receive a loading dose of phenytoin (15 mg/kg)
administered intravenously at a rate of not more than 50 mg per minute, with blood
17
pressure and ECG monitoring.
18
Stress ulceration and bleeding:
Medication to prevent stress ulceration of the stomach should be started on admission
in all patients who are unconscious and require intensive care. An H2-receptor
antagonist or a proton pump inhibitor should be administered intravenously.
Specific Management:
Antidotes:
Specific antidotes are available for only a small number of poisons.
Poison Antidote
Aluminium Desferrioxamine
Arsenic Dimercaprol (BAL), DMSA
Benzodiazepines Flumazenil
ß-adrenoceptor blocking drugs Atropine, glucagon
Copper Dimercaprol, D-penicillamine, DMPS
Cyanide Oxygen,dicobaltedetate,hydroxocobalamin, Sodium
thiosulphate
Digoxin and digitoxin Digoxin-specific antibody fragments
Ethylene glycol Fomepizole, Ethanol
Iron salts Desferrioxamine
Lead (inorganic) Sodium calcium edetate, DMSA
Methaemoglobinaemia Methylthioninium chloride (Methylene blue)
Methanol Fomepizole, Ethanol
Mercury (inorganic) DMPS
Opioids Naloxone
Organophosphorus compounds Atropine, Pralidoxime or obidoxime
Paracetamol N-acetylcysteine, Methionine
Thallium Prussian (Berlin) blue
Warfarin and other anticoagulants Vitamin K1
Dose of antidotes—annexure 3
Antidotes may exert a beneficial effect by:

Forming an inert complex with the poison (e.g. desferrioxamine, dicobalt edetate,
dimercaprol, DMSA, DMPS, digoxin-specific antibody fragments, hydroxocobalamin,
penicillamine, pralidoxime, protamine, Berlin (Prussian) blue, sodium calcium
edetate)

Accelerating the detoxification of the poison (e.g. methionine, N-acetylcysteine,
sodium thiosulphate)

Reducing the rate of conversion of the poison to a more toxic compound (e.g. ethanol,
fomepizole)

Competing with toxic substances for essential receptor sites (e.g. oxygen, naloxone,
vitamin K1)

Blocking essential receptors through which the toxic effects are mediated (e.g.
atropine)

Bypassing the effect of the poison (e.g. oxygen).
Reduction of Poison Absorption:
Inhaled:
19
To reduce poison absorption through the lungs, the casualty should be removed from the toxic
atmosphere, without the rescuers themselves being put at risk.
Skin:
If clothing is contaminated this should be removed to reduce dermal absorption. In addition,
contaminated skin should be washed thoroughly with soap and water.
Gut decontamination:
The efficacy of current methods to remove unabsorbed drug from the gastrointestinal tract
remains unproven. The two major international societies of clinical toxicology (American
Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres
and Clinical Toxicologists (EAPCCT)) have produced Position Statements on each method
and are quoted below.
Gastric lavage:
Gastric lavage involves the insertion of a large-bore orogastric tube into the stomach. Small
amounts (200-300 mL in an adult) of warm (38°C) fluid (water or 0.9% saline) are introduced
and removed by suction. Lavage is continued until the recovered solution is clear of
particulate matter. Gastric lavage should not be employed routinely in the management of
poisoned patients. The amount of marker removed by gastric lavage is highly variable and
diminishes with time. There is no certain evidence that its use improves clinical outcome and
it may cause significant morbidity. Gastric lavage should only be considered, therefore, if
a patient has ingested a potentially life-threatening amount of a poison and the
procedure can be undertaken within 1 hour of ingestion.
Gastric lavage can be given upto 4 hours in poisoning with salicylates, anticholinergic and
iron. Gastric lavage is contraindicated if airway-protective reflexes are lost (unless the patient
is intubated) and also if a hydrocarbon with high aspiration potential (e.g. Kerosine) or a
corrosive substance has been ingested.
Syrup ipecacuanha:
Syrup of ipecacuanha contains two alkaloids, emetine and cephaeline, which induce vomiting
by a central action and by a local action (emetine). Syrup of ipecacuanha should not be
administered in the management of poisoned patients. There is no evidence that it improves
the clinical outcome and therefore its administration, even in children, should be abandoned.
Single dose activated charcoal:
Activated charcoal has a highly developed internal pore structure which is able to adsorb a
wide variety of compounds and drugs, e.g. aspirin, carbamazepine, aminophylline, digoxin,
barbiturates, phenytoin, paracetamol. It does not absorb strong acids and alkalis, ethanol,
ethylene glycol, iron, lithium, mercury and methanol.
Single-dose activated charcoal should not be administered routinely in the management of
poisoned patients. Based on volunteer studies, the effectiveness of activated charcoal
decreases with time; the greatest benefit is within 1 hour of ingestion. The administration of
activated charcoal should only be considered if a patient (with an intact or protected airway)
has ingested a potentially toxic amount of a poison (which is known to be adsorbed to
charcoal) up to 1 hour previously. Again, there is no evidence that this improves the clinical
outcome.
Cathartics:
20
Whole bowel irrigation (WBI) requires the insertion of a nasogastric tube into the stomach
and the introduction of polyethylene glycol electrolyte solution 1500-2000 mL/h in an adult.
WBI is continued until the rectal effluent is clear.
WBI should not be used routinely in the management of the poisoned patient. Although some
volunteer studies have shown substantial decreases in the bioavailability of ingested drugs, no
controlled clinical trials have been performed and there is no conclusive evidence that WBI
improves the outcome of the poisoned patient.
Based on volunteer studies, WBI should be considered for potentially toxic ingestions of
sustained-release or enteric-coated drugs. There are insufficient data to support or exclude the
use of WBI for potentially toxic ingestions of iron, lead, zinc, or packets of illicit drugs; WBI
remains a theoretical option for these ingestions.
WBI is contraindicated in patients with bowel obstruction, perforation, ileus, and in patients
with haemodynamic instability or compromised unprotected airways. WBI should be used
cautiously in debilitated patients or in patients with medical conditions that may be further
compromised by its use.
Increasing Poison Elimination:
Treatments that might speed poison elimination are forced diuresis, urine alkalinization, acid
diuresis, multiple-dose activated charcoal, dialysis and haemoperfusion.
Forced diuresis:
The efficacy of forced diuresis depends on the poison being excreted unchanged by the
kidney or as an active metabolite. Most drugs are either degraded by the liver to non-toxic
metabolites or have such large volumes of distribution that there is insufficient active drug
elimination in urine for forced diuresis to be of any clinical value. The amount removed in
this way is insignificant compared to that removed by hepatic metabolism and forced diuresis
should not be used.
Urine alkalinization:
Most drugs, particularly unionized, lipid-soluble molecules, are largely reabsorbed by the
renal tubules. Increasing the concentration of ionized drug in the urine should reduce
reabsorption and further enhance elimination. This is achieved by manipulating urine pH
which enhances ionization and hence elimination of weakly acidic compounds such as
salicylates, phenobarbital, and chlorophenoxy herbicides. In practice, urine alkalinization is
only employed commonly in salicylate intoxication.
Urine acidification:
Although, theoretically, induction of urine acidification increases the elimination of basic
drugs such as amphetamines, there is no evidence that it is of clinical value in cases of
poisoning.
Multiple dose activated charcoal:
Multiple doses of activated charcoal aid the elimination of some drugs from the circulation by
interrupting their enterohepatic circulation and also by adsorbing the drug that has diffused
into the intestinal juices. The rate of transfer of the latter is dependent upon the blood supply
to the gut, the area of mucosa available for transfer, and the concentration gradient of the drug
across the mucosa. The adsorptive capacity of charcoal is such that as zero concentrations of
21
free drug are present in luminal fluid, the diffusion gradient still remains as high as possible.
The process has been termed 'gut dialysis' since, in effect, the intestinal mucosa is being used
as a semipermeable membrane.
Although many studies have demonstrated that multiple-dose activated charcoal increases
drug elimination significantly, this therapy has not yet been shown to reduce morbidity and
mortality. Multiple-dose activated charcoal should be considered only if a patient has
ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or
theophylline. In all of these cases there are data to confirm enhanced elimination, though no
controlled studies have demonstrated clinical benefit. Adults should receive 50-100 g
initially, followed by 50 g 4-hourly or 25 g 2-hourly until charcoal appears in the faeces or
recovery occurs.
Dialysis:
Haemodialysis in acute poisoning is most commonly indicated for the treatment of acute renal
failure and only infrequently to increase the elimination of poisons. The rate of elimination
across the dialysis membrane depends upon a number of variables including the molecular
weight of the poison, the extent to which it is protein-bound, the concentration gradient, and
pH of blood and dialysate. Haemodialysis is of little value in patients who ingest poisons with
large volumes of distribution, e.g. tricyclic antidepressants, because the plasma contains only
a small proportion of the total amount of drug in the body. Haemodialysis is indicated in
patients with severe clinical features and high plasma concentrations of ethanol, ethylene
glycol, isopropanol, lithium, methanol or salicylate.
Peritoneal dialysis increases the elimination of poisons such as ethylene glycol and methanol
but is much less efficient than haemodialysis.
Haemoperfusion:
This technique is not available routinely. It involves the passage of blood through an
adsorbent material, e.g. activated charcoal, but is no better than oral multidose activated
charcoal for the removal of phenobarbital, carbamazepine and theophylline. Other barbiturate
Do nots in poisoning:
and non-barbiturate hypnotics can be removed effectively but are now only rarely prescribed.
1. Do not give stomach wash with wide bore tube
2 .
No gastric lavage if ingestion >1hour. Except- salicylate,
iron and anticholinergic
3. No emesis
4. No forced dieresis except salicylate and amphetamine.
5 .
No whole bowel irrigation exception iron, lead, zinc and
packets of illicit drugs
22
Reference:
1. American Academy of Clinical Toxicology, European Association of Poison Centres and
ClinicalToxicologists. Position statement: ipecac syrup. J Toxicol Clin Toxicol
1997;35:699–709.
Clinical Toxicologists. Position statement: gastric lavage. JToxicol Clin Toxicol
1997;35:711–719.
Clinical Toxicologists. Position statement: single-dose activated charcoal. J Toxicol Clin
Toxicol 1997;35:721–741.
Clinical Toxicologists. Position statement and practice guidelines on the use of multi-dose
activated charcoal in the treatment of acute poisoning. J Toxicol Clin Toxicol
1999;37:731–751.
23
Chapter- 3
Organophosphorus Compound Poisoning
Duration: 01 hour 30 minutes
Lesson: 03
Objectives:
 Describe the pathogenesis, presentation & diagnosis of OPC poisoning.
 Assess the severity of illness.
 Tell the Principles of management of a case of OPC poisoning.
 Describe the outcome of OPC poisoning.
 Tell the diagnosis of atropinization
 Describe the toxicity of atropine & pralidoxime.
Sl
no
01 Ice breaking and

05min Presentation ,Question
Transparency/Flip
Introduction to the
and answer
chart
session
02 Pathogenesis,
15 min Presentation,
Multimedia,Board,Mar
presentation & diagnosis

discussion,
ker,
of OPC poisoning
Question and answer
Transparency/Flip
chart
03 Principles of
management of a case of
discussion,
ker,
OPC poisoning
Question and answer
Transparency/Flip
chart
04 Outcome of OPC
poisoning
discussion,
ker,
Question and answer

Transparency/Flip
chart
05 Approach of poisoning
15min Presentation,
management and
discussion,
ker,
atropinization
Question and answer
Transparency/Flip
chart
06 Toxicity of atropine &

pralidoxime
discussion,
ker,
Question and answer

Transparency/Flip
chart
07 Summarization 10 min Discussion,

Board, Marker,
Question and answer

Transparency/Flip
chart

05 min Question and answer Board, Marker, Flip

chart
participants
24
25
Introduction:
Organophosphorus compounds are widely used as insecticide in agricultural sector by the
farming community in Bangladesh used for the control of insect vectors. Since it is easy and
widely available, pesticide become a popular method of self harm. OP poisoning is one of the
most common cause of impulsive deliberate self - poisoning that the clinician frequently
encounter at different level of Hospital in Bangladesh.
The basic mechanism of toxic effects of organophosphates results from inhibition of
cholinesterase action at the nerve ending resulting in accumulation of excess acetylcholine.
So, combating the action of excess acetylcholine by rational use of atropine and oximes plays
a major role in management. However, the most suitable oximes for reactivation of
cholinesterase have still not been established with certainty, although pralidoxime is widely
recommended.
There is no universe consensus regarding diagnosis, grading of severity and management of
this serious life-threatening poisoning. Different individualized spectrum of management is
available around the world. The supportive and the specific antidotes are given and tuned
according to individual patient.
Substances Included in this Category:
There are more than a hundred organophosphate compounds used regularly.
Some available in Bangladesh include-
Chlorpyrifos Diazinon
Dichlorvos Dimethoat
Fenthion Malathion
Parathion
26
Clinical Features: Pesticide poisoning can be acute, sub-acute or chronic.
Acute poisoning: is from substantial intake of the toxicant in a single occasion which occurs
because of suicide attempts or accidental ingestion.
Sub-acute poisoning: is due to repeated smaller doses through penetration into the system
over a short period of time.
Chronic poisoning: refers to cumulative effect occurring from repeated exposure to small
amount of pesticides over a long period of time.
Acute, sub-acute or chronic poisoning may result from ingestion, absorption inhalation.
Fastest absorption takes place through eyes, scalp, back of the neck, forehead and scrotal
region. Inhalation of vaporized pesticides commonly takes place during mixing, handling or
spraying.
Pathogenesis:
Pathogenesis of Acute Cholinergic Crisis:
Organophosphates inhibit acetyl cholinesterase, an enzyme which itself inactivates the
neurotransmitter acetylcholine; the net effect being increased levels of active acetylcholine at
its various sites in the nervous system.
These locations include:

The neuroeffector junctions of the parasympathetic nervous system (and the
sympathetic nervous system in the case of the sweat glands)

The (autonomic) ganglia of both parasympathetic nervous system and sympathetic
nervous system

The neuromuscular junctions

Some synapses in the central nervous system
The increased neurotransmitter levels can result in increased target organ functional response,
or with sustained levels; a decreased response. The various effects have been classified as
Muscarinic, Nicotinic and Central effects.
OPC are known primarily as inhibitors of esterases. Phosphorylations of acetylcholinesterase
inhibits its catalytic function. The consequent accumulation of unhydrolysed acetylcholine
(Ach) at muscarinic, nicotinic and central sites of nervous system forms the pharmacological
basis of Acute Cholinergic Crisis (ACC). It may be mentioned that reactivation of inhibited
enzymes may occur spontaneously, the rate depends upon species and tissue, in addition to
the chemical group attached to the enzyme. This reactivation process may be induced by
some oxime agents but the response declines with time due to ageing of the inhibited
enzymes.
27
Fig: Nicotinic, muscarinic and central syndrome (courtesy- SACTRC, Srilanka)
Signs and symptoms of OPC poisoning:
Four clinical syndromes have been described

acute cholinergic symptoms and paralysis (most common)

subacute proximal weakness (Intermediate syndrome)

organophosphate induced delayed neuropathy (OPIDN)

chronic organophosphate induced neuropsychiatric disorder (COPIND)
Signs and symptoms of OPC poisoning:
Acute cholinergic crisis (ACC):
Muscarinic
Nausea, vomiting, abdominal cramps, diarrhoea, faecal

Gastrointestinal
incontinence

Respiratory
Pulmonary oedema, hypotension

Cardiovascular
Bradycardia, hypotension

Pupils
Blurring of vision, miosis

Urinary
Frequency, incontinence

Other
Increased sweating, salivation and lacrimation
Nicotinic
Muscle twitching, fasciculation, cramps, weakness including

Skeletal muscle
respiratory muscles

Sympathetic
Pallor tachycardia, hypertension
ganglion
CNS Giddiness, tension, anxiety, restlessness, difficulty in
concentration, confusion, slurred speech, insomnia, headache,
tremor, apathy, withdrawal and depression, drowsiness,
nightmares, ataxia, generalized weakness, coma, cheyne-stokes
respiration, convulsion, depression of respiratory and
circulatory centres.
Note: The mnemonic DUMBELS describes most of the significant muscarinic features
Diarrhoea Urination
Miosis Bronchospasm
Emesis Lachrymation
Salivation
28
29
Intermediate Syndrome (IMS):
IMS develop about 24-96 hours after OPI intoxication following ACC treated conventionally
or while on therapy in certain percentage of patients. Respiratory insufficiency may herald the
onset of IMS. The patient is usually conscious. Muscles innervated by cranial nerves show
varying degree of weakness. The external ocular muscles are most commonly affected,
producing ptosis and defects of ocular movements of mild to moderate severity. These may be
accompanied by weakness of muscles of mastication, face and soft palate. Weakness is
bilateral and symmetrical, therefore mild abnormalities may easily by overlooked. Weakness
of neck flexion often such that the patient cannot raise the head from bed is a constant feature.
The muscle tone in the limbs is usually normal but may be decreased. Shoulder abduction and
hip flexion show symmetrical weakness of varying severity. Normal power in the distal
muscles may give a false impression that the limbs are spared. Tendon reflexes are normal or
decreased. There is no sensory impairment.
Respiratory insufficiency develops over approximately 6 hours and initially the accessory
muscles of respiration are used. There is increased in respiratory rate, sweating, restlessness
and later cyanosis. If untreated the patient may soon become unconscious and die The
paralytic signs are 2 types. Type 1 (present on admission) and Type 2 (appearing subsequently
and not responding to atropine) the time of onset and the distribution of type 2 signs fit the
features of IMS.
Management – in the line of respiratory failure.
Delayed Polyneuropathy:
Organophosphorus induced delayed polyneuropathy (OPIDP) which occurs in a small
percentage of patients, manifests following a latent period of 2-4 weeks after exposure by any
route. It generally follows exposures sufficient to cause acute cholinergic symptoms ACC.
The cardinal symptoms are distal weakness and in some cases paraesthesia in the distal parts
of the limbs, foot drops, wrist drop and claw hands are inevitable consequences, Pyramidal
signs may appear after a few weeks or few months. Recovery is variable and the condition
may be permanent. Severe cases progress to complete paralysis, impaired respiration and
death.
Suggested diagnostic criteria include:

Symptoms and signs of polyneuropathy

Sometimes later pyramidal tract signs

Denervation changes (shown by electromyography)

Reasonable exclusion of other causes
Extra pyramidal manifestations
Atypical ocular bobbing, opsoclonus, cerebellar, choreo athetosis, chorea with psychiatric
changes and Parkinsonism following OP intoxication had been documented mostly as single
case reports.
Investigations: Not routinely needed. But can be done if needed.
a) Routine Laboratory Test:
Blood count -- Leucocytosis
Blood Sugar-- Hypoglycemia
LFT -- Increased PT
S. electrolytes-- Hypokalaemia
Urine -- Proteinuria
S. Amylase -- Raised
30
ECG -- Arrythmia
CXR -- Pulmonary oedema
31
Special test: If possible these tests can be done in OP poisoning.
1.
Direct measurement of OPC
2.
Indirect estimation of plasma & red cell Cholinesterases
3.
Estimation of NTE (Neuropathic transferase enzyme)
4.
Electrophysiological study
5.
Neurobehavioral test
6.
Histopathological test
7.
PEFR (Peak expiratory flow rate – Bed side)
8.
Spirometry
Sample of used offending pesticide or preferably container of pesticide as measure of
identification is very important in clinical setting. All patients and their attendants
should be repeatedly encouraged to bring the sample to the health facility for diagnosis
and management.
Grading of severity of poisoning:
a) Clinical grading
b) Biochemical Grading
The following table has been suggested as a guide to determining severity by South Asian
Cilinical Toxicology Research Collaboration. However if a patient has any CNS signs or
paralysis or has ingested a concentrated preparation, the poisoning is likely to be severe
irrespective of other initial signs.
Severity AChE
Muscarinic Nicotinic CNS
(RBC)
Mild > 40% nausea, vomiting,

headache,
diarrhoea, salivation,
dizziness
bronchorrhoea and
-constriction,
bradycardia
Moderate 20 - 40% as above, + miosis,

fasciculations
as above, +
incontinence
(fine muscles)
dysarthria, ataxia
Severe < 20% as above, +

as above, +
fasciculations
coma,
(diaphragm, resp.
convulsions
muscles)
32
Management of Organophosphorus Insecticide (OPC) Poisoning:
A patient of organophosphate poisoning should be hospitalized and the subsequent
management consists of:
1.
Initial stabilization of patient by maintaining respiration and other vital signs.
2.
Reduction of exposure.
3.
Administration of specific antidote.
4.
Supportive treatment.
Initial Stabilization of the patient:
The initial objective should be the establishment of a clear airway and adequate ventilation
because the patient with acute organophosphate poisoning (ACC) commonly presents with
respiratory distress secondary to excessive oropharyngeal secretion, bronchospasm,
respiratory muscle paralyis and rarely, acute respiratory distress syndrome and pulmonary
oedema. It is essential to improve tissue oxegenation as much as possible prior to
administration of atropine. In case of moderate to severe poisoning patients should be
managed in ICU if facilities are available.
Exposure reduction:
Thoroughly wash exposed areas, including axillae, groin, umbilicus, other skin folds, ears,
eyes, hair and under the nails; with soap and tepid water. Consider lavage only if a patient has
taken a highly toxic pesticide and arrives at hospital within 1–2 hours. There is currently no
evidence that either single or multiple dose regimens of activated charcoal result in clinical
benefit
There are two antidotes in the treatment of OPC poisoning:
Atropine- Is the antidote of choice which reverses the muscarinic features.
Oxime- Which reactivate cholinesterases inhibited by organophosphates and reverses the
nicotinic features.
Atropine:
Atropine acts as physiological antidote in all anti-cholinesterase intoxication. Atropine
antagonises the effects of acetylcholine reversing the excessive parasympathetic stimulation
by competing for identical binding sites at muscarinic receptors.
Dosage regimens of Atropine:
Patients poisoned by organophosphorus esters are tolerant to the pharmacological effects of
atropine and consequently very large doses are usually required. Repeated doses of atropine
should be administered until signs of atropinisation appear.
Signs of Atropinisation:

Mydriasis

Dry mouth & nose

Tachycardia.

Anhydrosis

Flushing

Bronchodilation
33
Dosage regimens are usually designed according to the severity of poisoning and to the
signs of atropinisation

1 ampoule contains 0.6 mg atropine sulphate.

Interval of atropine sulphate dose -every 5 min
Test dose of Atropine:
It is preferable to initiate the antidote therapy with a 'test dose' of parenteral atropine-
sulphate (1.2 mg in adults and 0.01 mg/kg in children, by the intravenous route). This
therapeutic test provides a measure of severity of organophosphate poisoning. If the signs
of atropinisation occur rapidly, it is unlikely that the poisoning is severe or it may not be
OP poisoning. However, these mildly poisoned patients who received a single dose of
atropine should be observed for at least 24 hours to detect further recurrence of toxicity
after the effects of atropine have subsided.
There is alternative therapy with atropine than current practice which have shown
excellent outcome as treatment and practiced in different south east Asian country
like Srilanka, Thailand etc. This practice is evidence based and strongly
recommended to follow for managing the organophosphate poisoning. The therapy is
described below:
Loading with atropine and IV fluids:
Dose of atropine
For an unconscious patient, give atropine 1.8–3 mg (three to five 0.6 mg vials) rapidly IV
into a fast-flowing IV drip. Although it is preferable that oxygen is given early to all ill
patients, do not delay giving atropine if oxygen is unavailable. Because atropine dries
secretions and reduces bronchospasm, its administration will improve patient oxygenation.
There is no good evidence that giving atropine to a cyanosed patient causes harm. Atropine
takes only a few minutes to work. During the 5 min after atropine administration, record
three other signs of cholinergic poisoning against which atropine dosing will be titrated
(Table 1): (1) air entry into lungs; (2) blood pressure; (3) heart rate.
There is no need to do this before atropine is given, because pinpoint pupils and sweating
in a region where these pesticides are common are sufficient to indicate OP/ carbamate
poisoning and trigger the decision to give atropine. If the clinical presentation is not clear,
administer atropine 0.6–1 mg. A marked increase in heart rate (more than 20–25
beats/min) and flushing of the skin suggest that the patient does not have significant
cholinergic poisoning and further atropine is not required.
34
Table 1: An observation chart recording the initial atropinisation of an organophosphorus-

poisoned patient
Initials
Study
Date of
XX
numbe
arrival
r
xx/xx/xx
Axxxx
Time Heart
Clear
Pupil
Dry
Syst.
Bowel
Confuse
Fever
Atropin
Bolus
rate
lungs
size
axilla
BP>80
sounds
d
(>37.5CC
e
given?
>80
mmHg
(ND/Nil
)
infusion
22.3
52 Creps+ Pinpoin
No 90/60 I No No 2.4 mg
0
t
22.3
60 Creps+ Pinpoin
No 90/60 I No No 4.8 mg
5
t
22.4
82 +/- Pinpoin
Yes 110/6
N No No 4mg
0
t
0
22.5
100 Wheeze 2 mm Yes - D No No 2mg
23.0
105 Clear 3 mm Yes - D No No 2 mg/h Infusio
0
n
23.1
105 Clear 3-4mm Yes - D No No 2 mg/h Infusio
5
n
23.3
102 Clear 3-4 mm Yes - D No No 2 mg/h Infusio
2
n
00.3
98 Clear 3-4mm Yes 110/6
D No No 2 mg/h Infusio
0
0
n
01.3
85 Clear 3-4 mm Yes - D No No 2 mg/h Infusio
0
n
02.3
72 Wheeze 3-4 mm Yes - N/D No No 2 mg
02.3
96 Clear 3-4 mm Yes - D No No 2.4 mg/h Infusio
5
n
02.4
5
n
04.0
0
n
{Atropinisation was reached at 23.00, 30 mm after the first atropine dose was given; a
total of 13.4 mg of atropine was required. After 10 mm, doubling doses were no longer
used because there was a clear response to therapy with the pulse climbing above 80
beats/mm and the chest sounding better. After a further 1.5 hours, the pulse rate started to
drop but it was not until it had dropped below 80 beats/mm and wheeze had become
audible in the chest that another 2 mg bolus was given to atropinise the patient again. The
atropine infusion rate was also increased and the patient remained stable for the next few
hours. AID/N/I, absent/decreased/normal/increased; creps,crepitations; syst. BP, systolic
blood pressure. Clinical features in bold type indicate that atropine is required. Dashes
indicate that no BP reading was taken.}
Giving fluids:
35
While waiting for the atropine to have effect, ensure that the two IV drips have been set up
(one for fluid and drugs, the other for atropine). Give 500–1000 ml (10–20 ml/kg) of
normal saline over 10–20 min.
Table 2: Target end-points for atropine therapy

Clear chest on auscultation with no wheeze

Heart rate >80 beats/min

Pupils no longer pinpoint

Dry axillae

Systolic blood pressure >80 mmHg
Notes:
1. The aim of atropine therapy is to clear the chest and reach the end-points for all five
parameters (Table-2).
2. There is no need to aim for a heart rate of 120–140 beats/min. This suggests atropine
toxicity rather than simple reversal of cholinergic poisoning. Such high heart rates will
cause particularly severe complications in older patients with pre-existing cardiac
disease – myocardial infarctions may result. However, tachycardia are also caused by
hypoxia, agitation, alcohol withdrawal, pneumonia, hypovolaemia, and fast oxime
administration. Tachycardia is not a contraindication for atropine if other features
suggest under atropinisation.
3. Aspiration will commonly result in focal crepitations. Attempt to distinguish such
crepitations from the more general crepitations of bronchorrhoea.
4. Splashes of organophosphorus into the eye will produce intense miosis that may not
respond to atropine therapy. However, symmetrical miosis is likely to be due to
systemic effects of the ingested pesticide.
Assess whether enough atropine has been given – is the patient atropinised?
Three to five minutes after giving atropine, check the five markers of cholinergic
poisoning (Table 2). Mark them on an OP/ carbamate observation sheet (Table 1). A
uniform improvement in most of the five parameters is required, not improvements in just
one. However, the most important parameters are air entry on chest auscultation, heart rate,
and blood pressure.
Pupil dilatation is sometimes delayed. and the other parameters may improve more rapidly,
it is reasonable to observe air entry on chest auscultation, heart rate, and blood pressure as
the main parameters for adequate atropinisation.. When all the parameters are satisfactory,
the patient has received enough atropine and is 'atropinised'.
Continuation of bolus atropine loading to reach atropinisation
If after 3–5 min a consistent improvement across the five parameters has not occurred,
then more atropine is required. Double the dose, and continue to double each time that
there is no response (Table 1). Do not simply repeat the initial dose of atropine. Some
patients need tens or hundreds of mg of atropine, so repeating 3 mg doses will mean that it
may take hours to give sufficient atropine. Severely ill patients will be dead by this point –
36
atropinise the patient as quickly as possible. Beware of pupils that do not dilate because
pesticide has been splashed into them directly, and lung crepitations that are due to
aspiration of the pesticide rather than the systemic effects of the pesticide. Generalised
wheeze may be a better sign of under-atropinization in a patient who has aspirated
pesticide.
37
Atropine treatment after atropinization
Once atropinised (with clear lungs, adequate heart rate [more than 80 beats/min] and blood
pressure [more than 80 mmHg systolic with good urine output], dry skin, and pupils no
longer pinpoint), set up an infusion using one of the two IV cannulae. This should keep the
blood atropine concentration in the therapeutic range, reducing fluctuation compared with
repeated bolus doses.
In the infusion, try giving 10–20% of the total amount of atropine that was required to load
the patient every hour. If very large doses (more than 30 mg) were initially required, then
less can be used. Larger doses may be required if oximes are not available. It is rare that an
infusion rate greater than 3–5 mg/ hour is necessary. Such high rates require frequent
review and reduction as necessary.
Observation of the patient
Review the patient and assess the five parameters every 15 min or so to see whether the
atropine infusion rate is adequate. As atropinisation is lost, with for example recurrence of
bronchospasm or bradycardia, give further boluses of atropine until they disappear, and
increase the infusion rate (Table 1). Once the parameters have settled, see the patient at
least hourly for the first 6 hours to check that the atropine infusion rate is sufficient and
that there are no signs of atropine toxicity. As the required dose of atropine falls,
observation for recurrence of cholinergic features can be done less often (every 2–3 hours).
However, regular observation is still required to spot patients at risk of, and going into,
respiratory failure.
Atropine toxicity
Excess atropine causes agitation, confusion, urinary retention, hyperthermia, bowel ileus
and tachycardia. During regular observation for signs of over treatment, check for the
features given in Table 2. The presence of all three suggests that too much atropine is
being given. Stop the atropine infusion. Check again after 30 min to see whether the
features of toxicity have settled. If not, continue to review every 30 min or so. When they
do settle, restart at 70–80% of the previous rate. The patient should then be seen frequently
to ensure that the new infusion rate has reduced the signs of atropine toxicity without
permitting the reappearance of cholinergic signs. Do not follow heart rate and pupil size
because they can be fast or slow, and big or small, respectively, depending on the balance
of nicotinic and muscarinic features. Tachycardia also occurs with rapid administration of
oximes and with pneumonia, hypovolaemia, hypoxia, and alcohol withdrawal, and is not a
contraindication to giving atropine. Catheterize unconscious patients soon after
resuscitation is completed. Look for urinary retention in an agitated confused patient;
agitation may settle after insertion of the catheter.
Table 3: Clinical features of Atropine toxicity
a) Peripheral effect
b) Central effect

Dry mouth

hyperpyrexia

Mydriasis

restlessness

blurred vision

anxiety

hot dry skin

excitement

tachycardia

hallucination

delirium

mania

cerebral depression
38
  coma
There is a American verbal felicity to describe a patient of atropine poisoning.

as hot as a hare

as blind as a bat

as dry as a bone

as red as a beet

as mad as a hen.
Special circumstances with atropine therapy
(a)
As atropine can induce ventricular tachycardia & ventricular fibrillation in a
severely hypoxic patient, hypoxia should be corrected before administration of
atropine. This is accomplished by artificial respiration & oxygen therapy.
(b)
As severely poisoning patients exhibit marked atropine resistance, they may require
up to 2-3 times the standard dose of atropine.
Oximes:
Although atropine is the excellent 'initiator antidote' in reversing the muscarinic effects of
OPC poisoning, it cannot ameliorate the nicotinic action & CNS effects and also cannot
reactivate the inhibited cholinesterase. For this reason, oximes are used in the
pharmacological management of OPC poisoning to ameliorate the nicotinic, muscarinic &
C.N.S. effects and to reactivate the inhibited cholinesterase.
Mechanism of Action of Oximes:
Oximes are the specific biochemical antidote for OPI intoxication.
They reactivate the inhibited cholinesterase by cleavage of phosphorylated active sites.
Oximes are effective only when the phsophorylated AchE has not undergone 'ageing'.
Pralidoxime (2-pyridine aldoxime or 2- PAM) is currently the most commonly used in
humans. Among the four salts of pralidoxime, (chloride, iodide, mesylate, methylsulphate)
pralidoxime chloride is the best because it has less side effects and chloride ion is more
physiological. Currently obidoxime has been introduced. It crosses blood brain barrier
more than pralidoxime.
Praliodoxime is used in conjunction with atropine in moderate and severe poisoning. It has
a strong synergistic effect with atropine and provides a dose sparing effect on the amount
of atropine. Pralidoxime is not equally effective against all organophosphates.
Dosage regimen of pralidoxime:
It is generally accepted that it should be given as early as possible but should not be
preceded by administration of atropine. The clinical benefit of oximes for OP pesticide
poisoning is not clear, being limited by the type of OP, poison load, time to start of
therapy, and dose of oxime.
Current WHO recommend giving a 30 mg/kg loading dose of pralidoxime over 10–20
min, followed by a continuous infusion of 8–10 mg/kg per hour until clinical recovery (for
example 12–24 hours after atropine is no longer required or the patient is extubated) or 7
days, whichever is later. Where obidoxime is available, a loading dose of 250 mg is
followed by an infusion giving 750 mg every 24 hours.
39
Treatment with pralidoxime should be continued, in conjunction with atropine, until there
is symptomatic improvement. The intramuscular route is acceptable if venous access is
difficult, particularly in convulsing patient.
Oximes are not recommended for carbamate poisoning.
Side effect of pralidoxime:
No significant side effects other than mild biochemical signs of liver toxicity, have been
observed in normal doses of pralidoxime using 1-2gm. intravenously but mild nausea and
vomiting have been reported in case of oral administration. Too rapid administration will
result in vomiting, tachycardia and hypertension (especially diastolic hypertension).
Administration of oximes may require reduction in the doses of atropine to avoid atropine
toxicity.
Pralidoxime Toxicity:
Very few cases of pralidoxime toxicity have been reported. Dizziness, blurred vision,
diplopia, headache, nausea and tachycardia have been reported if the rate of administration
exceeds 0.5 gm. per minute. However, very few of these features occur concurrently and
pralidoxime may be safely used, in the recommended doses, in cases of moderate to severe
poisoning.
Supportive Treatment of OPC Poisoning:
Administration of specific antidote or some emergency medicine doses not complete the
total management of OPC poisoning. A complementary and sometimes obligatory
supportive treatment constitutes the model of total management, which includes the
following:

Management of respiratory insufficiency.

Maintenance of circulation.

Treatment of convulsion and other complications.

Fluid and electrolyte balance.

Control of infections (aspiration pneumonia).

Maintenance of nutrition.

Control of body temperature.
Artificial Respiration:
As the clinical picture of OPC poisoning is dominated by respiratory insufficiency,
management of respiratory failure represents the corner stone of treatment. Artificial
ventilation should be started at the first sign of respiratory failure. For pulmonary oedema,
high concentration 02 therapy and diuretic should be used. Morphine and aminophlline
should be avoided. Broad spectrum antibiotic is used as prophylactic measure, especially
when there are chances of aspiration pneumonia, which sometimes complicates severe
OPC poisoning.
Diazepam:

Counteract CNS effects

Relieves anxiety

Antagonize convulsions

Improve morbidity and mortality
40
Dose of Diazepam: Adult: 10-20 mg. intravenously or subcutaneously
& also may be repeated as required
Children: 0.25-0.4mg./kg
Follow up of the patient:

Vital signs

Signs of Atropinisation

Effect of oxime

Toxicity of atropine and oxime

RBC and plasma AChE level

Recurrence of symptoms on withdrawal of antidote.

Restart the treatment promptly if recurrence occurs.

Patient’s general condition.
Cause of Death in OPC poisoning:
1. Immediate death:

Seizures.

Complex ventricular arrhythmias.
2. Death within 24 hours:
Attributable to the effect of organophosphate in acute cholinergic crisis in untreated
severe case

Respiratory failure.
3. Death within 10 days of poisoning:
Respiratory failure in treated case due to respiratory muscle paralysis in intermediate
syndrome
4. Late death:
Late death due to organophosphate poisoning has been described and is believed to be
secondary to ventricular arrhythmias, including Torsades de Pointes, which may occur
up to 15 days after acute intoxication.
Prognosis of Organophosphorus Insecticide Poisoning:
Deaths from severe organophosphate poisoning usually occur within the first 24 hours in
untreated cases and within 10 days in treatment failure cases. If there has been no anoxic
brain damage, recovery will usually occur within 10 days, although there may be residual
sequelae, which has been discussed before.
41
ALGORITHM: APPROACH TO THE MANAGEMENT OF POISONING DUE TO
ORGANOPHOSPHATE PESTICIDES
Suspected
External decontamination with water Remove clothing. Avoid
organophosphate Poisoning
contamination of other personnel. Gastric lavage / activated
charcoal/cathartics/assisted ventilation as appropriate
If cardiopulmonary arrest
Symptoms of
No symptoms of poisoning
occurs, resuscitate
poisoning occur
If rapid atropinisation occurs,

Atropine 1 mg in
Exposure
Exposure
poisoning may be mild.

adults, 0.01mg/kg in
likely
Unlikely
Check alternate diagnosis.

children
If atropinasation does not occur, repeat

Observe for 24-48 hours. Confirm
Observe for 24 hrs and
2mg-5mg atropine IV every 10-15

exposure and substance
discharge. Follow up as
appropriate
min(adult) or 0.02-0.05 mg/kg IV every
10-30 min (Children)

If no symptom occurs discharge
Confirm organophosphorus poisoning Confirm carbamate poisoning
Pralidoxime chloride 1-2g IV at max rate 0.5 g/min(adults),25- Continue atropine until symptomatic
50 mg/kg IV over 15-30 min(children).If no improvement,

improvement occurs
repeat after 1 hour, then every 8-12 hours or give IV infusion
upto 0.5g/h.
Continue atropine+ pralidoxime until symptomatic

Observe for 24-48 hours for late signs of
improvement and recovery of cholinesterases activity.

toxicity and discharge with appropriate
follow up
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344:665-671.
12. Eddleston M, Szinicz L, Eyer P, et al. Oximes inacute organophosphorus pesticide
poisoning: a systematic review of clinical trials. Q J Med 2002;95:275–283
43
44
Chapter- 4
Benzodiazepine Poisoning and Poisoning by Abusive Substances
Duration: 01 hour
Lesson: 04
Objectives:

Analyze history and clinical features related to
poisoning by benzodiazepines and few abusive
substances

Assess severity of poisoning by benzodiazepines
and few abusive substances

Provide emergency and continuing care, assess
referral need and provide follow-up care for
patients with poisoning by benzodiazepines and
few abusive substances.
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Benzodiazepine Poisoning:
Benzodiazepines (BZD) are commonly used for a variety of situations that include seizure
control, anxiety, alcohol withdrawal, insomnia, control of drug-associated agitation, as
muscle relaxants, and as pre-anesthetic agents. Because of their widespread popularity,
these drugs are commonly abused. In addition, BZDs frequently are used in overdose,
either alone or in association with other substances especially in suicidal attempt and
transport related poisoning.
The rate of onset of action is determined by rate of benzodiazepine absorption from the GI
tract. Benzodiazepine absorption is especially rapid when ethanol is present and the
stomach is empty. Peak blood concentrations of most agents occur within 1-3 hours.
Benzodiazepines are metabolized predominantly in the liver by oxidation and/or
conjugation. Most benzodiazepines are broken down into pharmacologically active
metabolites, which may have longer half-lives than the parent compounds.
Mortality/Morbidity:
Benzodiazepines are generally thought to be safe and death is rare. Mortality from a pure
benzodiazepine overdose is rare; it usually occurs in conjunction with concomitant alcohol
ingestion or use of other sedative-hypnotics. Intravenous administration or overdose of
ultrashort-acting benzodiazepines (eg, triazolam) is more likely to result in apnea and
death. Elderly individuals and very young persons are more susceptible to the CNS
depressant effects of benzodiazepines than people in other age groups. Intravenous
administration is associated with greater degrees of hypotension than other routes of
administration and occasional cardiac and respiratory arrest.
History: History should include the time, dose, and intent of the overdose. Determine if co-
ingestants are present and the duration of benzodiazepine use. Symptoms include –
Dizziness, Confusion, Drowsiness, Blurred vision, Unresponsiveness, Anxiety and
Agitation.
Physical: The physical examination should focus on the patient's vital signs and
cardiorespiratory and neurologic function. The frequently found physical signs are-
Nystagmus, Hallucinations, Slurred speech, Ataxia, Coma, Hypotonia, Weakness, Altered
mental status, impairment of cognition, Amnesia, Paradoxical agitation, Respiratory
depression and Hypotension
Workup: Qualitative screening of urine or blood may be performed but rarely influences
treatment decisions. Obtain an arterial blood gas if respiratory depression is present.
Following an intentional overdose, measure serum electrolytes, glucose, BUN, creatine
clearance, and acetaminophen concentration. Obtain a pregnancy test in women of
childbearing age. Obtain a chest x-ray if respiratory compromise is present. Evaluate for
aspiration. Evaluate for acute respiratory distress syndrome (ARDS). Obtain an
electrocardiogram (ECG) to evaluate for co-ingestants, particularly cyclic antidepressants.
Treatment:
Prehospital Care:

Supplemental oxygen

Intravenous access

Rapid blood sugar

Naloxone, if the diagnosis is unclear or an opiate co-ingestion is suspected
Emergency Department Care:

Continue supportive care and monitoring (e.g., cardiac monitoring, IV, oximetry,
vital signs).

Decontamination
47
o
Gastric lavage is not recommended but may be considered if the presence of
a lethal co-ingestant is suspected and the patient presents within 1 hour of
ingestion.
o
Single-dose activated charcoal is recommended for GI decontamination in
patients who present within 1 hours of ingestion or in symptomatic patients
when the time of ingestion is unknown.

Respiratory depression may be treated with assisted ventilation.
Medications:
Antidote:
Flumazenil is a selective competitive antagonist of the GABA receptor and the only
available specific antidote for benzodiazepines; it will reverse effects of benzodiazepines
but must be used with caution. In overdose situations, flumazenil may be used for patients
with pure benzodiazepine overdose who are verbally unresponsive and have no history of
long-term benzodiazepine use or seizure disorder. ECG should be performed before use to
confirm the absence of cardiac conduction disturbances (which would suggest the presence
of cyclic antidepressants). Use as a diagnostic and therapeutic agent for unsubstantiated
drug-associated coma is controversial. A positive response to small titratable doses may
obviate the need for endotracheal (ET) intubation and the search for other causes of coma.
The absence of clinical response to 2 mg of flumazenil within 5 to 10 minutes indicates
that benzodiazepines poisoning may not be major cause of CNS depression or coma.
The patient regains consciousness within 15 to 30 seconds after injection of flumazenil,
but since it is metabolised more rapidly than the benzodiazepines, recurrence of toxicity
and CNS depression can occur and the patient should be carefully monitored after initial
response to flumazenil therapy.
If the patient becomes unconscious again, flumazenil can be given by IV infusion 100-400
micrograms/hour rate being adjusted according to level of arousal.
Adult Dose: 0.1-0.2 mg IV q1min to a total dose of 1 mg at one time or 3 mg in 1 h;
infusion rates of 0.1 mg/min decrease disconcerting rapid arousal.
Pediatric Dose: 0.002-0.02 mg/kg IV q1min.
Contraindications:
Documented hypersensitivity; serious cyclic-antidepressant over dosage; patients using
benzodiazepines to control a potentially life-threatening condition (eg, intracranial
pressure, status epilepticus); chronic benzodiazepine use.
Pregnancy: category-C Safety for use during pregnancy has not been established.
Precautions:
Patients on benzodiazepines for prolonged periods may experience seizures; monitor for
resedation and unmasking of seizures
Abusive Substance Poisoning
People abuse substances such as drugs, alcohol, and tobacco for varied and complicated
reasons, but it is clear that our society pays a significant cost. Abused substances produce
some form of intoxication that alters judgment, perception, attention, or physical control.
Withdrawal of many of these can range from mild anxiety to seizures and hallucinations.
Drug overdose may also cause death.
Few abusive substances, their toxic symptoms and management are enumerated
below (alcoholic intoxication described elsewhere)–
Opiates: codeine, dihydrocodeine, morphine
48
Toxicity is enhanced if other CNS depressants such as alcohol are ingested as well.
Toxic dose: A toxic dose of opiate is difficult to assess as individual tolerances vary
greatly. Therefore, the following doses are to be interpreted with care: Codeine: 350 mg.
Dihydrocodeine: 420mg., Morphine: 30 mg (patients may be on higher doses in therapy;
the clinical effects may occur if established dose is exceeded). Overdoses may present with
nausea and vomiting. Some opioids may cause a rash, itching, flushing, drowsiness and
pinpoint pupils. Fensidyl, commonly used recreational medicine in Bangladesh, contains
high amount of codeine and dihydrocodeine.
In severe poisoning:

Unconsciousness, convulsions, hypotension.

Respiratory depression with cyanosis and respiratory arrest. Hypoxia due to
respiratory depression is the most frequent cause of death from opioid poisoning.
Serious complications include Non-cardiogenic pulmonary oedema, cardiovascular
collapse, and renal failure.
Management:

Activated charcoal can be given within 1 hour of ingestion to reduce absorption
unless the patient is drowsy, fitting or vomiting.

Naloxone can be given to reverse the signs of severe poisoning (coma, respiratory
depression or convulsions) within a few minutes but it has a short life and the
patient may relapse.

All patients who have taken an overdose of opioid analgesics should be transferred
to hospital and observed for at least 6 hours. Patients who require naloxone should
be observed for 24 hours. ECG monitoring and ventilation may be needed.
Marijuana (also known as ganja, grass, pot, weed, herb):
Marijuana comes from the plant Cannabis sativa. The plant produces delta-9-
tetrahydrocannabinol (THC), the active ingredient associated with intoxication. Marijuana
resin, called hashish, contains an even higher concentration of THC. The drug is usually
smoked, but it can also be eaten. Common effects of marijuana use include pleasure,
relaxation, and impaired coordination and memory. Often, the first illegal drug people use,
marijuana is associated with increased risk of progressing to more powerful and dangerous
drugs such as cocaine and heroin. It is virtually impossible to overdose from marijuana,
which sets it apart from most drugs.
Heroin (also known as smack, horse): Effects of heroin intoxication include drowsiness,
pleasure, and slowed breathing. Withdrawal can be intense and can include vomiting,
abdominal cramps, diarrhea, confusion, aches, and sweating. Overdose may result in death
from decreased breathing.
May present with:

Onset of effects within 30 minutes of ingestion or within seconds to minutes after
IV injection. The peak effects last for about 10–30 minutes and continue in milder
form for 2–4 hours.

Nausea, vomiting.

Dry mouth, constricted pupils, drowsiness, confusion, euphoria, a sense of
calmness, flushing, sweating and a feeling of warmth.
In severe cases:

Hypotension, coma, bradycardia, respiratory depression with associated
hypoxaemia and pulmonary oedema, cardiac arrhythmias. The pupils may be
dilated if hypoxic cerebral damage has occurred.
Management:
49


Naloxone can be given to reverse the signs of severe poisoning (coma, respiratory
depression or convulsions) within a few minutes, but it has a short life and the
patient may relapse.

All patients who have taken an overdose of opioid analgesics should be transferred
to A&E and observed for at least 6 hours. Patients who require naloxone should be
observed for 24 hours. ECG monitoring and ventilation may be needed.

Adult dose 0.4mg, can be repeated at intervals of 2-3 minutes to a maximum of
10mg. (Naloxon ampoule, 0.4mg/ml).
Tricyclic antidepressants:
Includes: amitriptyline, amoxapine, clomipramine, dothiepin, doxepin, imipramine,
lofepramine, nortriptyline, protriptyline and trimipramine.
Although the individual TCAs have differences in side-effects and kinetics, most behave
similarly in an acute overdose. Peak plasma levels normally occur within 2–8 hours of a
therapeutic dose because of delayed gastric emptying. After an overdose, peak levels may
occur even later. Life-threatening signs usually develop within 6 hours of ingestion or not
at all. The complications most often associated with a fatal outcome are severe
hypotension and cardiac arrhythmias.
Toxic dose:

Hospital observation is recommended for ingestion > 5 mg/kg.

10-20 mg/kg can be life threatening.

Anticholinergic effects, sedation and hallucinations can occur at doses
< 5 mg/kg.
May present with:

Dry mouth, dilated pupils, urine retention, hallucinations, jerky movements,
drowsiness.

Metabolic acidosis and hypokalaemia.

Coma, hypotension, hypothermia, convulsions, respiratory depression, pulmonary
oedema, cardiac arrhythmias, cardiac arrest. Arrhythmias may not respond to
therapy.

Lofepramine is less likely to cause cardiac effects.

Amoxapine is more likely to cause arrhythmias and convulsions.
Management:
The greatest risk of seizures and arrhythmias occurs within the first 6-8 hours of cyclic
antidepressant (TCA) ingestion. The treatment of an asymptomatic patient with a history
of CA ingestion is mainly supportive therapy. For all patients with possible TCA toxicity,
airway protection, ventilation and oxygenation, intravenous fluids, cardiac monitoring, and
performing ECG are all essential measures.
Consider early gastric decontamination using charcoal if the patient presents within 1 hour
of ingestion.
Once suicidal ideation is ruled out and the patient remains asymptomatic for 6-8 hours
postingestion without any ECG changes, the patient may be discharged home. If suicidal
ideation is present, evaluation for admission to a psychiatric facility is mandatory.

Airway: Endotracheal intubation may be necessary in patients who present with
seizures or who are in a comatose state for airway protection.

Hyperventilation: The use of hyperventilation is controversial. It has been
recommended traditionally for the resultant alkaline state hyperventilation
50
achieves. Alkalinization is thought to increase protein binding of TCA and promote
TCA excretion, thereby decreasing cardiotoxicity.

Hypotension
o Normal saline intravenous fluids are indicated for TCA-induced
hypotension.
o
For hypotension refractory to intravenous saline, vasopressors with alpha-
agonist effect (eg, Neo-Synephrine, norepinephrine) may be used.

GI decontamination: Once the patient is stabilized, activated charcoal can be
considered.

Intravenous sodium bicarbonate
o
Serum alkalinization with intravenous sodium bicarbonate has been the
mainstay of therapy in TCA-induced cardiovascular toxicity. Prolonged
QRS is most often the indication for serum alkalinization in TCA toxicity.
Not all physicians agree on what the duration of QRS should be in order for
them to institute intravenous sodium bicarbonate therapy. However, about
88% of the poison control directors in the United States use a QRS of 100
milliseconds or greater as the cut off for intravenous sodium bicarbonate.
Evidence suggests the reversal of toxic effects of TCA (eg, QRS
prolongation, myocardial depression) following serum alkalization and
sodium loading with sodium bicarbonate.

Benzodiazepines: The seizures in TCA toxicity are usually self-limited. The
treatment of choice for prolonged or recurrent seizures in TCA toxicity is a
benzodiazepine.

Hemodialysis or hemoperfusion: Because of the large volume of distribution and
high protein-binding characteristics of TCAs, hemodialysis has not been shown to
be effective in the treatment of TCA overdose.
Sodium bicarbonate
First-line therapy for QRS interval >100 milliseconds or if dysrhythmias are present.
Correction of acidosis promotes protein binding of TCA and improves myocardial
contractility. Doses or IV drip may be administered with a pH goal of 7.5-7.55. Monitor
and replace potassium as needed to prevent hypokalemia.
Adult: 1-2 mEq/kg bolus IV; IV drip of 3 amps of sodium bicarbonate in 1 L of D5W to
maintain a pH of 7.45-7.55
Pediatric: Administer as in adults
Cocaine (also known as crack, coke, snow, rock):
Derived from the coca plant of South America, cocaine can be smoked, injected, snorted,
or swallowed. Desired effects include pleasure and increased alertness. Short-term effects
also include paranoia, constriction of blood vessels leading to heart damage or stroke,
irregular heartbeat, and death. Severe depression and reduced energy often accompany
withdrawal. Both short- and long-term use of cocaine has been associated with damage to
the heart, the brain, the lung, and the kidneys.
The fatal dose of cocaine has been approximated 1.2 g, although severe toxic effects have
been reported from doses as low as 20 mg.
Symptoms:
The symptoms of cocaine poisoning are referable to the CNS, namely the patient becomes
excited, restless, garrulous, anxious and confused. Enhanced reflexes, headache, rapid
pulse, irregular respiration, chills, rise in b.p, temperature, mydriasis, exophthalmos,
51
nausea, vomiting, and abdominal pain are noticed in severe overdoses, delirium, Cheyne-
Stokes respiration, convulsions, unconsciousness and death from respiratory arrest result.
Acute poisoning by cocaine is rapid in developing.
Treatment:
The specific treatment of acute cocaine poisoning is the intravenous administration of a
short-acting barbiturate or diazepam. Artificial respiration may be necessary. It is
important to limit absorption of the drug. If entrance of the drug into circulation can be
checked, and respiratory exchange maintained, the progress is favorable since cocaine is
eliminated fairly rapidly.
Amphetamine and MDMA (ecstasy)
MDMA is an amphetamine derivative. It is taken as a tablet or powder enclosed in a
capsule. Adverse effects more commonly occur after ‘recreational’ doses rather than with
an overdose.
May present with:

Onset of symptoms from amphetamine according to the route of exposure.

Transient nausea, increased muscle tone, muscle pain, trismus (jaw-clenching),
dilated pupils, blurred vision, sweating, dry mouth, agitation, anxiety, palpitations,
vomiting, abdominal pain and diarrhoea.

Hypertonia, hyper-reflexia, hyperpyrexia, tachycardia, initial hypertension then
hypotension, tachypnoea, and visual hallucinations.

Effects may be prolonged if a patient has alkaline urine.

Delirium, coma, convulsions and cardiac dysrrhythmias that may be fatal.

A hyperthermic syndrome may develop with rigidity, hyper-reflexia and
hyperpyrexia (>39°C) leading to hypotension, rhabdomyolysis, metabolic acidosis,
acute renal failure, disseminated intravascular coagulation, hepatocellular necrosis,
adult respiratory distress syndrome and cardiovascular collapse.

Death from intracerebral haemorrhage has also been reported in hyperthermic
patients.

MDMA is also associated with hyponatraemia and cerebral oedema. This can occur
in patients who have consumed excessive amounts of water (owing to drug-

induced repetitive behaviour). These patients present with mild hypothermia and
confusion; they may be unresponsive and staring.
‘Yaba’ is acombination of methamphetamine and caffeine. Yaba, which means crazy
medicine in Thai, is produced is Southeast and East Asia. Yaba is produced as tablets.
These tablets are generally no larger than a pencil eraser. They are brightly colored, usually
reddish-orange or green.
Yaba has recently emerged as a drug of abuse among the young int affluent societies in
Bangladesh. Individuals who use Yaba face the same risks as users of other forms of
methamphetamine: rapid heart rate, increased blood pressure, and damage to the small
blood vessels in the brain that can lead to stroke. Chronic use of the drug can result in
death. Individuals who use Yaba also may have episodes of violent behavior, paranoia,
anxiety, confusion, and insomnia.
Management:

52

All patients should be transferred to hospital and observed for at least 6 hours with
electrocardiogram (ECG) monitoring and the monitoring of electrolytes balance

Give diazepam for convulsions.

If the rectal temperature > 39°C, instigate cooling measures (fan, sponging, ice
packs, cool IV fluids). If this is unsuccessful, the patient will need to be paralysed
and ventilated.
Follow-up:
Further Inpatient Care: Admit patients with hemodynamic instability, coma, or
respiratory depression to the ICU. Watch for signs of withdrawal in patients who have
been taking BZDs chronically before overdose.
Further Outpatient Care: Patients may be discharged if they remain asymptomatic 4-6
hours postingestion. Those with mild toxicity may be observed in the emergency
department until they recover.
Transfer: Transfer patients who may require more advanced care than is available in
inpatient setting.
Other Complications of abusive drugs:
 Aspiration pneumonia
 Rhabdomyolysis
 Fatality (rare)
Treatment of Complications:
CNS stimulation may require sedation, usually with a benzodiazepine or a barbiturate. In
pure amphetamine poisoning, chlorpromazine or a benzodiazepine may be used. To
terminate seizures or prevent their recurrence, a benzodiazepine (eg, diazepam 5 to 10 mg
for adults; 0.1 to 0.2 mg/kg for children) is given slowly IV, or Phenobarbital (100 to 200
mg IV or IM for adults; 4 to 7 mg/kg for children) is given. Ideally, phenytoin is avoided.
O2 saturation should be closely monitored. Refractory seizures very rarely, if ever, require
general anesthesia.
Severe CNS depression requires circulatory and ventilatory support. Endotracheal
intubation and, rarely, tracheostomy may be necessary. In suspected or known narcotic
poisoning, naloxone should be used in repeated doses. Stimulants are ineffective and are
generally contraindicated.
Cerebral edema is common in poisoning due to sedatives, carbon monoxide, lead, and
other CNS depressants. A 20% mannitol solution (5 to 10 mL/kg) is given slowly IV over
30 to 60 min. Corticosteroids are also used (dexamethasone 1 mg/m2 of BSA q 6 h by IV
drip). Intracranial monitoring with hyperventilation to try to alter the degree of cerebral
edema is used less frequently.
Renal failure, if present, may require dialysis.
Hepatic failure may warrant transplantation.
Medical/Legal Pitfalls:
a.
Unmasking an underlying disorder, specifically seizures, with indiscriminate use
of flumazenil
b.
Failure to anticipate withdrawal in a patient with chronic BZD use
c.
Failure to consider the possibility of co-ingestant use or secondary causes of
treatable altered mental status (eg, hypoglycemia, meningitis).
53
Reference:
1.
Meredith TJ et al. “Naloxone, flumazenil and dantrolene as antidotes”. IPCS/CES
Evaluation of antidotes series 1993;1 :27-44
2.
Wei-Ber Liao et al. “Anticholinergic overdose induced torsade de point
successfully treated with verapamil”. Japanese Heart J 1996; 37: 925 – 931.
3.
Henderson RA et al. “Life threatening ventricular arrhythmia (Torsades de
pointes) after haloperidol overdose”. Hum & Exp Toxicol 1991; 10: 59 – 62.
4.
Pond SM et at. “Randomized Study of the Treatment of Phenobarbital Overdose
With Repeated Doses of Activated Charcoal”. JAMA 1984; 251 (23): 3104 – 8.
54
Chapter- 5
Corrosive Poisons
Duration: 01 hour
Lesson: 05
Objectives:
 Classify the types of the corrosive poisoning.
 Describe its pathogenesis.
 Identify the sign/symptoms and to establish the
diagnosis.
 Manage and treat the case.
 Identify and manage the complications of corrosive
poisoning and
 Describe its medico legal importance.
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Introduction:
Any chemical when ingested causing tissue injury to the gastrointestinal mucosa may
termed as caustics- which are also known as corrosive poisons-i-e. strong acids locally
produce corrosion and tissue necrosis, when they come in contact. They coagulate tissue
proteins; fix the tissue, extract tissue fluid, and if the person survives for a reasonable
period, then there is ulcer formation, sloughing of the necrosed tissue and scar formation
with contracture.
Mineral acids and alkalies (corrosive agents) have direct local action, but may have
indirect action, when ingested and absorbed in the system viz, circulatory and respiratory
systems. Organic corrosive agents cause direct local and remote action as they are
absorbed and reache to the different systems.
Classification:
According to chemical action, corrosive agents may classify as:
Corrosive Poison
A) Strong Acids B) Strong Alkalis

C)Metallic Salts
a) Zinc Chloride
b) Pot. Cyanide
c) Ferric Chloride
Inorganic
d) Chrometes of Alkalies
e) Bicarbonates of Alkalies
Organic
a. Sulphuric acid
b. Nitric acid
a) Carbolic acid g) Creosotes
c. Hydrochloric acid
b) Acetic acid h) Tetrodotoxin
d. Hydrofluoric acid
c) Oxalic acid I) Tetro terrado toxin

Hydroxides
d) Tartaric acid j)Hydrochloric acid
e) Picric acid j) Hydrofluric acid

a) Sodium Hydroxide
f) Salicylic acid
b)Potassium Hydroxide
c)Ammonium Hydroxide
d. Hydrofluoric acid
Mode of Action:
When ingested, moderately strong acids produce coagulation necrosis of the gut mucosa,
and formation of Escher limits the damage up to the superficial layers, while alkalies cause
liquifactive nercosis of the mucosa with saponification and continued deeper penetration
into the underlying tissues causing extensive damage.
In both strong acids and alkalies, tissues immediately become corroded, soft and some
times dissolved, disintegrated and perforated and thus the whole or part of it, or part of the
intestine turns into a small soft pulpy mass.
Acids:
Domestic Use: Many of acids are used in various household products like toilet. Bowl
cleaner. Metal cleaner, antirust compound, battery fluid and pool sanitizer. Industrial use
of acids includes electroplating, photography, calico printing, rayon manufacturing and in
different chemical laboratory.
A)
Sulphuric acid: It is a colourless, heavy, oily, odourless hygroscopic liquid. It
causes brittle chalky white teeth, ulceration of the mouth, oesophagus and stomach,
where there may be perforation followed by generalized peritonitis.
57
Vitriolage: Throwing of the corrosive substance specially sulphuric acid ( Oil of
vitriole) on any person usually on the face for disfiguration due to enemity or
rivality is called vitriolage, which is a grievous hurt and a punishable offence.
B)
Nitric acid: Pure nitric acid is a clear, colourless, pungent choking odour liquid
and emits white fumes when exposed in open air. Locally it is corrosive agent
causing yellow colouration of the teeth and produce respiratory distress.
C)
Hydrochloric acid: Pure hydrochloric acid is a volatile colourless, odourless
(Liquid) having burning sour taste. Shock usually occur due to severe pain. There
may be no significant change in the teeth.
Oxalic acid: It is a colourless transparent prismatic crystals and sour in taste. It is
D)
used in calico printings, manufacturing of straw hats, removing ink from the paper
and cloths, removing rust stains from the metallic and wooden articles and
preparation of various pickles and chanachurs. Its common clinical features are
feeble pulse, cold and clammy skin, low blood pressure and shallow respiration.
Coma and death due to asphyxia followed by respiratory failure.
E)
Acetic acid: It is a colourless liquid with sour taste and pungent smell. In
concentrated form it is corrosive, but in diluted form it is irritant. Vinegar contains
4-5% acetic acid.
F)
Picric acid: Locally it produces corrosion with tissue necrosis. When ingested, it
causes muscular cramping, drowsiness, stupor, decomposes red blood cells, meth-
haemoglobinaemia and irritate CNS following convulsion coma and death. In low
dose it causes cramping pain in the stomach, yellow vomiting, diarrhea of yellow
liquid stool, yellow colouration of the skin and conjunctiva, dilatation of pupil with
marked dehydration. Urine first becomes dark yellow, then turns into ruby red
colouration with dysuria, even anuria.
G)
Formic acid: When ingested it produces cramping pain in the stomach, petechieal
haemorrhage, intravascular haemolysis, disseminated intravascular coagulalation,
severe acidosis, renal failure etc.
Carbolic acid: It is a dark magenta coloured liquid with a typical phenol odour.
H)
Carbolic acid poisoning (Carbolism) includes- hot burning pain extending from the
mouth to the stomach. Skin- becomes cold and clammy with subnormal
temperature. Pupil constricted, feeble thready pulse, hypotension, slow laboured
stertorous respiration with convulsion and lock jaw. Oliguria or anuria may be
present. Urine contains albumin, blood casts and metabolic products i.e.
hydroquinone and pyrocatechol- colouring the urine Olivo green-known as
carboluria.
58
Summary feature of acid poisoning:
Skin contact with acid causes pain, blistering, ulceration and lacerating necrosis, with
severe scarring after weeks.
Ingestion by mouth causes immediate pain with pharyngeal edema and burns. Pain and
mucosal edema causes difficulty in swallowing. Features of pharyngeal involvement
includes hoarseness, stridor, respiratory distress and laryngeal and/or epiglottic edema.
Perforation of the esophagus and/or stomach may occur, which can lead to chemical
peritonitis. Abdominal pain, vomiting, diarrhea and haematmesis occur in more severe
cases. Systemic effect includes circulatory collapse, metabolic acidosis, hypoxia,
respiratory failure, intravascular coagulation and hemolysis. Renal failure occurs as the
end result of ATN. Later effect of acid ingestion includes pyloric stenosis, stricture
formation and achlorohydria.
Grading system for corrosive burns of the alimentary tract with endoscopy:
Grade Features

1 Erythema and oedema only

2a Localized,superficial friability,blistes or ulceration

2b Features as for grade 2a,but with circumferential ulceration

3 Multiple deep ulcers,area of necrosis
Diagnosis is based on the history of exposure
Management and treatment:
1.
Emesis should not be induced.It is contraindicated.
2.
Attempt at gastric lavage is contraindicated due to danger of perforation.
3.
Dilution and /or neutralization is also contraindicated
4.
Steroids confer no benefit & may mask abdominal sign of perforation
5.
Early endoscopy as soon as possible.
6.
Inj Morphine / Diclofenac sodium for pain
7.
Soluable calcium tablet for hydrofluric acid ingestion if patient able to swallow
followed by I.V. Inj. of 10% calcium gluconate 10ml with I.V. infusion of
dextrose in normal saline.
8.
Oxygen inhalation and artificial respiration if necessary.
9.
For external burn and eye injury wash immediately with water or saline for 10
to 30 minutes. Then use oint silver sulphadiazine for skin, and chloramphenicol
eye point for eye.
10.
For oedema of the glottis- tracheostomy should be done.
11.
Surgery: For esopheseal stricture and gastric outlet obstruction. Usually done
after 4-6 weeks of ingestion.
12.
Management of complications (e.g. peritonitis) if any.
Alkalis:
Sodium Hydroxide (Caustic soda) is a constituent of oven and drain cleaners and
dishwashers.
Sodium carbonate (washing soda) having strong alkaline taste is less toxic than potassium
carbonate.
Potassium hydroxide (caustic Potash) is a soapy viscid in touch, used in hearing aid
batteries.
Potassium carbonate is a white crystalline powder having a caustic and alkaline taste used
as a cleaning and washing agent.
59
Bleach: Common house hold bleach has 3-6% of sodium hypochlorite. Its PH is about 11,
more of which cause oesophagial ulceration.
Detergents: Most of the detergents contain sodium tripolyphosphate and sodium
carbonate which are weakly alkaline and usually do not produce significant toxicity.
Ammonium hydroxide- contains 32.5% of ammonia and is used at home for removing
paint, oil and dirt usually from the clothing.
Clinical Features:

Alkali damage to the oesophagus may produce diffused blurred oesophageal
mucosul ulceration, sloughing, with petechial haemorrhagic spottings throughout
the whole mucosa and its underlying tissues. Perforation of gastric or intestinal
wall is less common. Oesophageal perforation can develop and as its sequel
medistinitis pneumonitis, cardiac injury and tracheo oesophageal & aortico-enteric
fistula may ensue.

Metabolic acidosis may develop in patients with severe gastrointestinal bleeding.

Renal failure is a rare complication, may be accompanied by Gl bleeding and
shock.

Inhalation of alkaline vapour may cause hoarseness,stridor,upper airway oedema,
wheezing, pneumonitis and respiratory failure.

Ocular exposure may produce severe conjunctival irritation, chemosis, corneal
epithelial defects, limbal ischemia and permanent visual loss may occur in severe
cases.

Dermal contact with alkaline corrosives may produce redness, irritation, pain and
sometimes-full thickness burns of the skin.
Diagnosis: Is based on history of the exposure and P H of the collected gastric lavage.
Management/ Treatment:
1.
Dilution or neutralization, induce emesis, gastric aspiration and lavage are
contraindicated.
2.
Irrigate exposed eyes with sterile cold water or saline at least for 20 minutes and
continue until the P H returns to normal.
3.
Emulcents- egg white, olive oil, butter, cold milk should be avoided.
4.
Clear air way and support with O2 inhalation and artificial respiration, if necessary
intensive care unit support including ventilator.
5.
I.V. fluid for maintaining nutrition and electrolyte balance.
6.
As there is no specific antidote for alkaline corrosives, symptomatic treatments are
to be done. Neutralisation with alkali now-a-days is not done.
7.
Surgical treatment must be considered for any patient with grade II or III
esophageal injury.
8.
Analgesia including Narcotics,or NSAID (Inj. Diclofenac) may be given to relieve
pain
9.
Diagnostic endoscopy should be performed within 12-24 hrs of alkali ingesion.
10.
Corticosteroids have no role in the management of a case and complication. It is
rather harmful.
Medico legal importance:
1.
Usually accidental poisoning due to over dose
2.
Suicidal poisoning very rare
60
3. Homicidal Poisoning not adopted
61
Reference:
1.
Meredith T. “Corrosives”. Med International 1995; 9: 25 – 27.
2.
Munoz Munoz E et al. “Swallowing of hydrochloric acid: study of 25 cases”. Rev
Esp Enferm Dig 1998.; 90 (10: 701 – 7.
3.
Pelelova D, Navratil T. “ Do corticosteroids prevent oesophageal stricture after
corrosive ingestion”? Toxicol Rev. 2005; 24 (2): 125-9.
4.
Ertrkin C et al. “The results of caustic ingestions- Hepatogastroentrology” 2004; 51
(59): 1397 – 400.
62
Chapter- 6
Hydrocarbon (Kerosene) Poisoning
Duration: 01 hour
Lesson : 06
Objectives:
 Tell the magnitude of kerosene poisoning.
 Explain the Patho-physiology of kerosene poisoning
 Tell the important clinical features of kerosene poisoning
 Describe the management of kerosene poisoning
 Describe the complication of kerosene poisoning and its prevention
 Tell the supportive measures
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Background informations:
Poisoning with kerosene one of the commonest forms of acute childhood poisoning in
many developing countries. Kerosene ingestion occurs mainly during the summer months
and predominantly affects children between ages of 1 to 5 years. Many of these children
come from lower socio-economic group and rural areas. In Dhaka Medical College
Hospital 4-6% of total admission in the pediatric department consists kerosene poisoning.
Kerosene is available in most homes where it is used as cooking fuel and for lighting. In
household it is normally kept in bottles especially mineral water bottle, fruit and soda
bottles; and kept at the ground level without any safety cap; which attracts children, who
think that they are drinking their usual beverage.
Mode of Poisoning:

Mostly accidental.
Patho-physiology:
In general, lower the viscosity and higher the volatility of the hydrocarbon compound,
greater the pulmonary toxicity. Kerosene is the volatile hydrocarbon and is inhaled into
lungs as the child is drinking it and during vomiting or gastric lavage. When ingested it is
readily absorbed from the stomach and excreted by the lungs. Inhalation into and excretion
from the lungs produce a chemical pneumonitis and pulmonary oedema. Hydrocarbon may
interact with pulmonary surfactant, resulting in alveolar collapse. Cyanosis developed
quickly, due to (1) displacement of alveolar gas by vaporised hydrocarbon (2)
Bronchospasm due to irritation may contribute to the ventilation perfusion abnormalities
with resultant hypoxia. Aspiration of even 0.2 ml of kerosene can produce chemical
pneumonitis. Encephalopathy is believed to be secondary to hypoxia.
Fatal dose: 30 ml
Fatal period: 24 hours (usually)
Clinical features:
(a)
Asymptomatic.
(b)
The ingestion of kerosene immediately produces burning sensation in the mouth
and pharynges as well as nausea and vomiting.
(c)
Kerosene odour in the breath and vomitus.
(d)
Fever: Within hours, there may be temperature elevation (38-400
c) but subsides
within 24-48 hours and does not warrants antibiotic treatment. If temperature rises
after 48 hours it indicates infection and antibiotic is warranted.
(e)
Most common manifestation is respiratory symptoms and may be present within 30
minutes; progression occurs over the first 24 hours and subsides between 2-5 days.
While it is less extensive aspiration, the onset of pulmonary symptoms and
inflammation may be delayed 12-24 hours. Pulmonary symptoms are varying
64
degrees of cyanosis, tachycardia, tachypnoea, nasal flaring as well as
supraclavicular, intercostal retraction and chest-indrawing. Features of
bronchospasm, consolidation, crackles may be present. Hypoxemia may be present
and be assessed by pulse oximetry.
(f)
Nausea, vomiting, abdominal pain and diarrhea by increasing peristalsis.
(g)
Encephalopathy may range from lethergy to convulsion and coma.
(h)
Rare cases may developed myocarditis.
(i)
The inhalation of other hydrocarbons may produce dyspnoea, fever, severe hypoxia
and bilateral pulmonary infiltrate.
Causes of death:
(a)
The usual cause of death is respiratory failure.
(b)
Rarely by ventricular arrhythmia.
Diagnosis:
(a)
History of kerosene ingestion
(b)
Smell of kerosene in the breath, mouth and body
(c)
Fever, respiratory symptoms and / or CNS manifestation
(d)
Investigations:
1)
X-ray chest-Radiological evidence of pneumonitis occurs in 62-89% of
cases, and may be seen as early as 30 minutes after ingestion but may not be
apparent until 6-12 hours. X-ray changes were graded as follows-

Grade-0: Normal X-ray.
Grade-1: Minimal unilateral perihilar infiltration.
Grade-2: Bilateral infiltration.
Grade-3: Confluent fluffy shadows on one or both sides.
Grade-4: Extensive bilateral infiltration with consolidation &/or pleural
effusion.
2)
Pulse oximetry-O2 saturation.
3)
Total count of WBC-Leukocytosis.
Management:
All patients should be hospitalized for at least 24 hours irrespective of severity.
A. Asymptomatic cases: Admit for observation and discharge after 24 hours if no
symptom develops.
B. Symptomatic cases: Patients who are symptomatic when they are first examined,
patients who become symptomatic during 24 hours observation should be managed
according to following guideline.
(a) Evaluate and maintain the ventilatory status of the patients. Administration of 02 to
all patients with respiratory symptoms, some patients (respiratory failure) may
require intubation and ventilatory support.
(b) If the skin has been exposed to kerosene, remove all contaminated clothing and
wash the skin with copious amounts of water.
(c) The routine use of antibiotics is not recommended, the occurrence of secondary
infection of the affected lung can usually be readily detected by re-appearance of
fever on 3rd to 5th day after ingestion.
(d) Other supportive treatment: Nutritional support.
65
(e) Corticosteroid, activated charcoal, cathartics, mineral oil and olive oil have no
beneficial effect.
Complications:
(a) Immediate
• Pneumothorax
• Subcutaneous emphysema
• Empyema
• Pneumatocele usually developes in the recovery phase of the pneumonitis and
causes no impairment of the respiratory functions. These resolved slowly and it
may take 6-9 months for their complete resolution.
• Secondary infection with bacteria or virus.
(b) Long term
• Some patients develop persistent cough or frequent respiratory infection.
• Increased risk of developing chronic lung disease as adults when exposed to risk
factors e.g. smoking, air pollution.
Prognosis:
Prognosis depends on a variety of factors, including the volume of the ingestion or
aspiration, the specific agent involved and the adequacy of medical care. Most children
survive without complication or sequelae. Some progress rapidly to respiratory failure and
death.
Decision rule for referral:
Not all the cases at the rural level will need higher care at the secondary and tertiary level.
A simple decision rule may help the primary care physician to segregate the cases
requiring referral and keeping the rest for home care and/or observation at the THC. This
decision rule is recommended by the WHO-EMRO.
If any child within 2 hours after kerosene ingestion presents with the any of the following
the child should be referred to higher center for further care-

1.
Wheeze
2.
Tachypnea
a.
Age 2 up to 12 months: ≥50 / min
b.
Age 12 months up to 5 years: ≥40/min
3.
Altered mental state:
a.
Restless or Irritable
b.
Lethargic
c.
Unconscious
Prevention:
By taking following specific measures
• Storage of kerosene in designated containers above ground level out of reach of
children
• Emphasis on adult supervision of children
66
Algorithm of management of kerosene poisoning in hospital
Hydrocarbon (Kerosene) poisoning
Removal of contaminated clothes and wash
(No emesis or gastric lavage)
CNS manifestation
Respiratory symptoms
(Restless/ irritable, somnolence, convulsion, coma)

(cough,respiratory distress, tachypnoea,
1.
Measures of unconscious patient
cyanosis, features of consolidation,
2.
Anticonvulsant
pleural effusion,etc.)
 Inj. diazepam-0.5 mg/Kg/dose PR/IV or

Inj. Phenobarbiton Loading 15-20 mg /Kg
I/V Maintenance 5-6 mg/Kg/day 12 hourly

Yes
No
3.
Nutritional support
Observe 24 hours
4.
Maintain fluid and electrolyte balance
Resp. symptoms,
CXR finding
(-)ve (+) ve
Discharge Hospitalization & Active
Management
Supportive measures
1. Control temperature
2. O 2 inhalation if there is hypoxia.
3. Bag and mask ventilation, intubation and mechanical ventilation if
there is resp failure
4. Nutritional support
5. IV fluid
6. When infection is suspected Injection Ampicillin 200 mg/Kg/day 6
hourly for 5-7 days, Metronidazole may be added for 5 days.
7. Steroids have no beneficial effect
67
Chapter – 7
Copper Sulphate Poisoning
Duration: 45 minutes
Lesson : 07
Objectives:
 Explain the mechanism of copper sulphate
poisoning.
 Tell the clinical features and diagnosis
 Describe the management
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Introduction:
Copper sulphate is a blue, crystalline or granular powder. Its anhydrous form is white in
colour. It is used as fungicide, algicide, herbicide, molluscide and also in steel and
petroleum industry. In Bangladesh copper sulphate poisoning occurs mostly in Southern
region. There was high mortality of this poisoning compare to other forms. It is cheap and
widely available in rural shop and devoid of significant pungent smell or bad taste. Farmer
and fisherman use it for skin diseases
Mechanism of toxicity:
Copper inhibits enzymes, G-6-PD and glutathione reductase, which are important in
protecting the cell from oxygen free radicals, lipid peroxidation. Significant increases of
copper content in the mitochondrion suggest hepatic mitochondrion to be an important
target in hepatic toxicity, with an involvement of oxidant damage to the liver. Hemolysis is
produced by the increased oxidation of hemoglobin sulfhydryl groups, leading to increased
red blood cell permeability.
copper toxicity occurs in the order by the erythrocytes, the liver and then the kidneys.
Intravascular haemolysis appears after 12-24h, Jaundice appears on the second or third day
and Renal complications are usually seen on the third or the fourth day after ingestion of
C.sulphate.
Toxic dose: ingestion of 250 mcg can cause toxicity and 10-20 mg is lethal. The lowest
oral toxic dose reported is 120microgm/dI. Serum copper level above 500microgm/dI are
associated with severe toxicity (normal range 89-137microgm/dl in males and 87-153
microgm/dl in female). Severe hepatic disorder has been reported in children after
ingestion of 10mg of copper in contaminated milk.
Clinical features:

Ingestion causes abdominal pain, nausea, vomiting, diarrhea, (characteristic blue
green), salivation and metallic taste, hematemesis and melaena.

Stools, vomitus, saliva, and mucous membrane are often stained green or blue.

Extensive corrosion and necrosis of GIT may take place.

Jaundice due to both hemolysis as well as direct liver damage may be present. It
may cause tender hepatomegaly. There is a reported case of hepatic encephalopathy

Intravascular hemolysis and hemoglobinuria occur 12-14 hrs after ingestion

Oliguria and renal failure can occur due to direct toxicity as well as intravascular
hemolysis.

Methaemoglobinaemia may be produced. Severe methemoglobinemia can result in
cardiac dysryhtmia and hypoxia which could contribute significantly to
cardiovascular collapse. Cardiac abnormalities was reported with multiple
ventricular extrasystloes, tachycardia and occasional unifocal bigeminy particularly
in paediatric group of patients. It can be happened even within 10 hours of
consumption of the poison.
69
 Hypotension and hypothermia may occur.

In severe cases seizures, delirium and coma may occur. Complete paralysis of
limbs is rarely observed.

It can cause dermal irritation on contact.
Diagnosis:
Diagnosis is based on history of exposure. Inhalation of copper fumes is associated with
fever and respiratory complaints.
Laboratory/Monitoring:
1. Baseline haemoglobin, liver function, renal function and electrolyte levels should be
obtained and monitored as clinically indicated until symptoms abate.
2. Haemoglobin should be monitored as clinically indicated to guide the need for blood
transfusion.
3. Monitoring renal functions and electrolytes is required to assess the fluid status and
extent of renal failure and sometime to asses the renal toxicity of chelating agents like
penicillamine.
4. In patients with hepatitis and bleeding manifestations, coagulation parameters have to be
monitored.
But for the resource poor settings Hb. Estimation and S.creatinine is most important for
better management and prognosis.

Monitor whole blood copper levels in symptomatic patients.

Estimate methemoglobin levels in cyanotic patients.

Obtain chest X ray.
Management:
Pre hospital:

Do not induce emesis.

Irrigate exposed eyes or skin with copious amount of water.
Hospital

Provide supportive care.

Perform gastric lavage if present within one hour.

Treat shock with IV fluids and vasopressors as needed, blood transfusion if needed.

D-penicillamine : Adult dose: 1000 to 1500 mg/day divided every six to 12h,
before meals. The idea is to maintain the dose ,timing of administration is variable.

Paediatric dose: Initially 10 mg/kg/day, gradually increase to 30 mg/kg/day
divided in two or three doses as tolerated. Doses up to 100 mg/kg/day in four
divided doses; maximum one gram/day may be used depending on the severity of
poisoning and adverse effects.
Avoid in patients with penicillin allergy. Proteinuria, hematuria, renal failure,
bone marrow suppression and hepatotoxicity are the common adverse
effects.
70

Intramuscular BAL is appropriate in patients in whom vomiting and
gastrointestinal injury prevents oral D-penicillamine administration. BAL- copper
complex primarily undergoes billiary elimination and hence it is useful in patients
with renal failure. Dose: 3 to 5 mg/kg/dose deep intramuscularly every four hours
for two days, every four to six hours for an additional two days, then every four to
12h for up to seven additional days. Adverse reactions are urinary and persistent
hyperpyrexia.
Both the drug has similar effectiveness , so for resource poor settings like us any one of the
above two is fine.

Inj Omeprazole/Ranitidine may be given to treat GIT erosions.

Inj Oradexon may be given to prevent acute haemolysis of RBC. The most suitable
group to receive corticosteroid (with antibiotic) is probably the patients with grade
IIb injuries in endoscopy (submucosal lesions, ulcerations and exudates with near
circumferential injuries). In patients with grade III ulcers (deep ulcers and necrosis
into periesophageal tissues) stricture formation occurs, irrespective of steroid
administration. Moreover, steroids may mask or worsen the complications of
corrosives in grade III patients and hence steroids are contraindicated

Blood transfusion is needed to correct anaemia in severe cases.

Treat methemoglobinemia with methylene blue and humidified `supplemental
oxyzen.

Treat hepatic failure & renal failure.
References:
1. Mehta A,Patney NI, Bhati DPS, Singh SP. Copper Sulphate poisoning, J Ind Med
Assoc.1985; 83:108-10
2. Kurisaki E, KSuroda Y, Sato M. Copper-binding protein in acute copper poisoning.
Forens Sci Int 1988;38 :3-11.
3.Azhar MA, Rahman MA,Rashid HU. Acute renal failure following copper intoxication
and its reversal after dialysis. Bang Renal J.1985; 4:19-20
4. H.A.M Nazmul Ahsan, M A Jalil Chowdhury, M A Azhar, A F M Rafiquddin
Coppper sulphate poisoning, Tropical doctor. 1994; 24: 52-3
71
Chapter – 8
Aluminium Phosphide Poisoning
Lesson : 08
Objectives:
 Explain the mechanism of Aluminium
Phosphide poisoning.
 Tell the clinical features and diagnosis
 Describe the management
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Introduction:
Aluminium phosphide is a rodenticide widely used for grain preservation. It is hydrolyzed
by the acid in the stomach to form phosphine, which is very toxic. It is also used in
fumigation as tablet form. Fumigant tablets commonly available in Bangladesh and India as
quick fume
Mode of Action:
The exact mechanism is not known. It is suggested to produce non-competitive inhibition of
the cytochrome oxidase of mitochondria, blocking the electron transfer chain and oxidative
phosphorylation producing an energy crisis in the cells. (Cherfuka W et al.1976)
Recently Chugh et al. found inhibiton of catalase and induction of SOD in
humans leading to free radicals stress brought out lipid peroxidation and protein denaturation
of cell membrane leading to hypoxic cell damage
The multi-organ failure and shock are likely to be due to direct cytotoxic oxidative
damage. Damage to the heart, lungs, and the vasculature will then have secondary
contributing effects due to resultant hypoxia and hypoperfusion. Similarly damage to the
gut and lungs may lead to secondary opportunistic infections.
Fig. (A), (B) Aluminium Phosphide (Quick Fume tab.)
Clinical Features
Ingestion:
73
Nausea, vomiting, abdominal pain and headache are the early symptoms observed after
ingestion. Tightness of the chest, dyspnoea, cough, pulmonary oedema, excitement,
agitation and thirst are the other features.
Oliguria, anuria, abdominal dysfunction, jaundice, bleeding tendencies, metabolic acidosis,
convulsions, cardiac dysrrhythmias, and shock are the manifestations of severe poisoning.
Aluminium phosphide ingestion may give rise to persistent hypotension.
Inhalation
Inhalation can cause vomiting, diarrhoea, fever, cyanosis and tachycardia .
Mild to Moderate Phosphide Toxicity Moderate to Severe Phosphide Toxicity
Nasal irritation
Hypotension
Eye irritation
Metabolic acidosis
Cough
Hypokalemia
Headache
Severe dyspnea
Fatigue
Gastrointestinal bleeding
Nausea
Jaundice
Vomiting
Hypomagnesemia
Abdominal pain
Cardiac dysrhythmias
Chest tightness
Cardiac failure
Dizziness
Pulmonary edema
Ataxia
Coma
Seizures
Emergency Monitoring:
Pulse
Cardiac rhythm
ECG (12 lead)
Blood pressure
Level of consciousness
Respiration
Oximetry
Acid base balance
Serum electrolytes (especially potassium, calcium, phosphate, magnesium)
Serum creatine kinase (CK-MB fraction if myocardial ischemia is suspected)
Plasma cardiac troponin T (if myocardial ischemia suspected)
Following phosphide ingestion, phosphine can be detected in the expired air using silver
nitrate impregnated filter paper or strips, which blacken. This can also be used to test
gastric aspirate.
Management:
There are no proven antidote for Aluminium phosphide.
Perform gastric lavage. Use, if available, 1:5000 potassium permanganate solution or 2%
sodium bicarbonate solution.
Advise strict bed rest.
74
Maintain a fluid balance chart. Give adequate oral or IV fluids. Correct acidosis with
sodium bicarbonate IV.
Estimate serum electrolytes and correct any imbalance. Correct shock with infusions of
adequate IV fluids, plasma or whole blood.
If hypotension does not respond to adequate IV fluids, raise the foot end of the bed. Give
dopamine. If still no response, give hydrocortisone 400 mg IV 4 hourly or dexamethasone 4
mg IV 4 hourly.
If dyspnoea is present give 100% oxygen.
Give vitamin K 1 (phytomenadione) 10 mg IV daily, if prothrombin time is prolonged.
Test for hepatic and renal function. Anticipate and treat hepatic and renal failure.
Prognosis:
Despite adequate management mortality is very high.
Reference:
1. Surjith Singh et al. "Aluminium phosphide ingestion - a clinico-pathologic study".
Clin Toxicol 1996: 34; 703-706.
2. Clinical information Data Base (Poison information centre, Srilanka)
3. www.toxinz.com
75
Chapter-9
Methanol Poisoning
Lesson: 09
Objectives:

Identify methanol, its different forms that are used in household
and industries
 Explain the mechanism of toxicity

Describe Clinical features, fatality and diagnosis of Methanol
poisoning
 Tell the management and medico-legal importance
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Introduction:
Methanol is methyl alcohol also known as wood-alcohol or wood neptha synthesized from
coke and water. It is a colourless water soluble liquid with a typical aromatic odour and
slightly bitter taste. Industrial methyllated spirit consists of 95% ethyl alcohol and 5%
methyl alcohol. Mineralised methylated spirit contains 90% ethyl alcohol and 10% methyl
alcohol. Surgical spirit contains 95% ethyl alcohol and 5% methyl alcohol in which oil of
wintergreen is added for sweetish aromatic flavour for easy detection and pleasant use.
It is used in many home chemicals, duplicating fluids, varnishes, stains, paint thinners and
dyes. Methylated spirit is very cheap and frequently available; hence it is easily adulterated
and used as country liquor- among some Bangladeshi, Indian, Pakistani and Srilankan poor
peoples who cannot afford ethyl alcohol for their drink.
Absorption, distribution and excretion:
The specific gravity of methanol is 0.81 (ethanol is 0.79), i.e. one liter contains 810gm of
methanol. It is rapidly absorbed from the intestine and to a small extent from the stomach.
Its rate of absorption is more than glucose. The absorption depends upon concentration
(The higher the concentration, the rapid absorption) and condition of the stomach (in
empty stomach-rapid absorption) and is completed within 3 hours. If the concentration is
below 20% it increases gastric secretion.
After absorption, from blood it mostly goes to the intracellular and extra cellular fluid of
the tissue and less to body fat. When the absorption completed, urine and CSF contains
20% more alcohol than blood. Ninety Percent of the alcohol is oxidized in the liver. Rest is
excreted through urine and exhaled air. Its oxidation and excretion are much slower than
ethyl alcohol. In presence of ethyl alcohol its absorption, metabolism and excretion are
further delayed.
Mechanism of Toxicity (Metabolism):
Methanol itself is less toxic agent. It becomes highly toxic when it is mixed with ethyl
alcohol as it is adulerated. The rate of oxidation is very slow, only about 15% of that of
ethyl alcohol. When taken with ethyl alcohol, it is metabolized only after complete
metabolisation of ethyl alcohol. In course of oxidation, formaldehyde and finally formic
acid are formed which are highly toxic. Ethyl alcohol is preferentially metabolized by
alcohol dehydrogenase resulting in reduced methanol toxicity.
Action, Clinical Features and Fatality:
A) CNS Toxicity: It depresses CNS causing headache, dizziness, vertigo, dyspnoea,
cyanosis, cardiac depression and muscular weakness. It is less respiratory depressant
than ethyl alcohol, but its delayed effects are very dangerous which includes optic
nerve atrophy resulting in complete blindness. The delay of developing toxicity may
require 6-72 hours, but usually between 12-24 hours.
B) Ocular toxicity: It is a delayed feature, which includes blurring of vision, which
gradually leads to total or partial blindness. On examination pupillary dilatation, retinal
oedema and hyperemia of the optic disc may be found. Twenty percent of the victims
become totally blind, others have different form of visual disabilities.
77
C) Renal Toxicity: There may be scanty micturition, which is acidic and contains acetone
and formate; sometimes there may be total anuria.
D) GIT toxicity: It includes nausea and abdominal pain. About 40% of the methanol users
have high amylase level.
E) Respiratory toxicity: There may be dyspnoea, respiratory distress and death is usually
due to respiratory failure.
Laboratory Diagnosis:
a. Methanol poisoning causes an elevated osmolar gap, which may be detected by the
difference between the measured and the calculated osmolarity. Osmolarity is
calculated by the formula: Osmolarity= (2 X Na) + (BUN/2.8) +(Glucose/18). A serum
level of 200mg/dI of methanol adds approximately 62 mosm/L to the osmolar gap.
b. Methanol also produces high anion gap acidosis, which is due to excessive production
of formic acid and lactic acid.
Management:
The intoxicated person must be hospitalized and kept under close observation, even after
initial recovery. He must be treated by an ophthalmogist for his visual problems. Other
managements are:

Stomach wash although advocated, there is no evidence of effectivity with it.

Oxygen inhalation and artificial respiration in moderate cases

In severe case patient should be intubated and mechanical respiration should be
given.

Circulation should be maintained by giving fluids and sympathomimetics

Maintaining fluid electrolyte balance should combat dehydration. Acidosis should
be controlled by infusing sodium bicarbonate- which is essential if the pH<7.35 or
bicarbonate < 15 meq/I.

Renal failure should be monitored carefully.

Sedation can be given cautiously to prevent delirium and restlessness.

Eyes should be protected from light and should be under regular observation.

Ethyl alcohol therapy is given to delay the absorption and metabolism and thus to
prevent damaging effect of methanol:

The antidote for methanol poisoning is ethanol. Absolute alcohol is suitable for IV
use. Ethanol is given orally or IV to maintain a blood ethanol level of 100 to 150
mg/dI. This will block methanol metabolism. In mild poisoning, oral ethanol is
adequate. Give 10% ethanol 7.5 ml/kg IV, over 30 to 60 minutes, as a loading dose.
The recommended maintenance dose for non-drinkers is 10% ethanol 1 ml/kg/hr
IV. For chronic ethanol drinkers, the maintenance dose is 10% ethanol 1.96
ml/kg/hr IV. If the patient is undergoing hemodialysis, the maintenance dose is 3
ml/kg/hr. (A solution of about 10% ethanol can be made by mixing 60 ml of
absolute alcohol suitable for IV use in 500 ml of 5% dextrose).

Ethanol can be administered orally if the IV preparation is not available.
Concentrations less than 20% are preferred to avoid gastric irritation. A loading
dose of 95% ethanol, 0.8 ml/kg followed by 0.1 mI/kg/hr can be given. If the
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patient is undergoing hemodialysis, increase the dose up to 0.2 ml/kg/hr and
administer via a nasogastric; tube. For chronic ethanol drinkers, the maintenance
dose is 0.2 ml/kg/hr. The alcohol should be diluted in water or fruit juice.

If no alcohol is available in the hospital, give arrack (Gin, or whisky) 1.8 mI/kg as
a loading dose, and 0.2 ml/kg/hr as maintenance dose orally, after diluted with
water or fruit juice. If the patient is undergoing haemodialysis, the maintenance
dose is 0.7 ml/kg/hr.Dose: should be loading with 50gm of 50% ethyl alcohol (e.g.
125 ml of gin, whisky or vodka) orally followed by further oral dose for 3-4 days or
an intravenous infusion of 10-12 g ethanol/hour, to achieve a blood concentration
of about 500-1000 mg/litre. Ethanol should be given until methanol is undetected
in the blood. A serum ethanol level of 1 00mg/dI is essential to achieve the best
counter effect of methanol. For chronic ethanol drinkers, the maintenance dose is
0.45 ml/kg/hr.
In calculating the parenteral doses, it must be remembered that ethanol has a
specific gravity of approximately 0.8 (i.e. 95% ethanol is approximately 76 g/100
ml and not 95 g/100 ml).
The above regimes should be maintained for 2 to 3 days, unless contraindicated for any
reason, or until plasma methanol concentration is less than 20 mg/dI.
Blood ethanol level should be monitored hourly initially, and at longer intervals thereafter,
depending on the facilities available.
As prolonged ethanol administration can cause hypoglycaemia, especially in children,
determine blood glucose levels and give glucose orally or 5% or 50% dextrose IV.
If convulsions are present give diazepam 5 to 10 mg IV (Paediatric dose: 0.2 mg/kg).
Repeat if necessary.
Hemodialysis or peritoneal dialysis is effective in removing the absorbed poison and its
metabolites.
Indication for dialysis:
1) Has ingested more than 30 gm methanol
2) Develop metabolic acidosis or mental, visual or fundoscopic abnormalities
attributable to methanol
3) Has a blood methanol concentration > 500mg/litre.
Hemodialysis is more effective than peritoneal dialysis. If dialysis is used, increased
quantities of ethanol (17-22 g/hour) must be administered.

Use of 4- methylpyrazole (Fomepizole) is a direct inhibitor of alcohol
dehydrogenase. Dose: Loading dose 15mg/kg body wt over 30 minute, four 12
hourly doses of 10mg/kg should be given until the methanol concentration is less
than 200mg/litre. In case of dialysis 4 hourly doses is required as it is dialyzable.

Folinic acid, 50 mg i.v. 4 hourly may protect against ocular toxicity by accelerating
formate metabolism.
Medico-legal Importance:
Most of the poisoning is accidental, due to adulteration with methylated spirit and other
narcotics, but post mortern reports always go in favour of suicide as it is selfly taken.
Homicide is very much uncommon.
Reference:
1.
Roy M et at. “ What are the adverse effects of ethanol used as an antidote in the
treatment of suspected methanol poisoning in children” J. Toxicol Clin Toxicol
2003; 41 (2): 155-61.
79
2.
Meyer RJ et al. :Methanol Poisoning: . N Z. Med J 2000; 113 (1102): 11-3.
3.
Bowden CA, Krenzelok EP. “Clinical application of commonly used contemporary
antidotes”. Drug safety 1997; 16: 26-28.
80
Chapter -10
Dhatura Poisoning
Lesson: 10
Objectives:
 Identify Dhatura plant and its different forms used for poisoning
 List their route of administration, pathogenesis and signs-
symptoms
 Describe the treatment of Dhatura poisoning
 Explain the medico legal importance of Dhatura poisoning.
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Introduction:
Dhatura plants abundantly grow all over the tropical countries of the world, especially in
the waste and wild places. Even by the side of the country roads of Bangladesh, India,
Pakistan and Sri Lanka. These herbal plants are bush formed & 3-4 ft height having
alternate and broadly ovate leaves, long bell shaped flowers and spherical small apple like
spiky fruits-also known as thorn apple.
They are of two common families.
1 . Dhatura fastuosa - Dhatura alba, Dhatura nigra.
2. Dhatura stromorium.
Dhatura fastuosa are the common and most available plants found in our country-
having two varieties.
The seeds of dhatura are kidney shaped, yellowish brown in colour having bitter taste but
odorless, having similarity with capsicum seeds. Each fruit contain about 500 seeds.
Alkaloids of Dhatura and their medicinal use:
All parts of the plant are poisonous but fruits and seeds are more toxic. The active toxic
alkaloids include-
a) Hyoscine
b) Hyoscyamine and
c) Traces of atropine.
All of the alkaloids in therapeutic dose produce relaxation of smooth muscle and atropine
produces mydriasis.
Route of administration; absorption and excretion:
Orally:
The alkaloids are well absorbed through the mucus membrane of the G.I tract
and respiratory tract.
a.
Seeds are crushed and mixed with sweets, drinks and vegetables.
b.
Seeds and leaves are mixed with tobaccos & ganja and smoked.
c.
Usually decoction is added to some drinks to enhance its toxicity.
The absorbed toxin is distributed throughout the whole body by circulation within half an
hour. Large part of the absorbed poison excreted through urine without any change. Some
part of the poison undergo oxidation in the liver. The excretion usually completed within
10-24 hours.
Mechanism of actions of Dhatura:
The alkaloids block the acetylcholine by competitive antagonism and thus produce
sympathomymetic or parasympatholytic actions.
Signs and symptoms:
a)
Local contact produce allergic skin rash with itching & dermatitis.
b)
When taken orally- Symptoms usually appear within half an hour. (1) Bitter taste,
(2) Dryness of the mouth, (3) Difficulty in deglutition, talking and dysphagia, (4)
Vomiting due to gastric irritation. (5) Burning pain in the stomach and throat, (6)
Voice becomes hoarse (7) Giddiness , (8) Staggering gait, (9) Inco-ordination of
muscles like a drunk, some times muscular spasm, (10) Peculiar flushed
appearance of the face, (11) Dry hot skin with rise of temp. upto 1060 f or above
(12) laboured respiration (13) Congested red conjunctiva, (14) Marked dilated
83
pupils (15) Loss of accommodation for near objects, (16) Drowsiness, (17) Scarlet
rash or exfoliation of skin, (18) Pulse is full and bounding but in later stage it
becomes weak, irregular and intermittent, (19) Delirium of peculiar character,
c)
In early stage-excitement and purposeless talkativeness and incoherence with
restlessness. He may be silent or mutters inaudible and indistinct words but usually
noisy and tries to run away from the bed and tries to pickup the bed cloths or pull
some imaginary threads from the tip of his fingers and is subjected to dreadful
hallucinations of sight and hearing, (20) In fatal cases stage of excitement soon
subside and followed by stupor, convulsion and sinks into deep sleep or coma
within ½ - 1½ hours. Patient may remain in this stage for 1-2 days, but in most of
the cases (21) Death occurs due to sudden respiratory failure within 24 hours.
For easy memorise-10 “D” may be the symptoms of Dhatura poisoning. (1) Dryness of the
mouth (2) Dysphagia, (3) Dry hot skin (4) Dysarthria, (5) Diplopia, (6) Drunken gait (7)
Dreadful hallucination (8) Dilated pupil, (9) Delirium and (10) Drowsiness.
On the other way dhatura poisoned person may be described as-
(a) Dry as a bone (anhydrosis, urinary retention, decreased bowel movements)
(b) Red as a beet (Flushed face, cutaneous vasodilatation).
(c) Blind as a bat (Mydriasis, ciliary muscle paralysis)
(d) Hot as a bird/hare (raised temp. due to cutaneous vasodilatation).
(e) Mad as a wounded bear. (CNS arousal, agitation).
Fatal Dose- Usually 70-110 crushed seeds, 6-10 seeds may cause stupefaction.
Fatal period -18-24 hours, shortest being 6 hours.
Management:
 Stomach wash: with plain water if patient presented within one hour of intoxication.
 Respiratory distress should be checked by repeated cleaning of the airway passage
(described in general management section).
 Specific antidote : (i) Physostigmine 0.5 mg to 1 mg S/C to antagonise atropine in
asingle dose, (ii) Prostigmine is more effective and less toxic than physostigmine in
same dose. (iii) Pilocarpine 5 mg S/C. though useful, does not counteract the action of
dhatura on brain, can be repeated 2 hourly at early stage of poisoning.
 Delirium can be treated with short acting barbiturate.
 To control marked excitement chloral hydrate or paraldehyde in moderate dose may
be given.
 For hyper pyrexia- cold sponging to be done and antipyrexic drugs like paracetamol
can be given through rectal or oral route.
 Light diet, mainly liquid or semi solid should be given if the condition is mild and pt
is conscious.
84
 Catheterization done for urinary retention.
Medicolegal importance:
(i) In most cases crushed dhatura seeds are used by the road snatchers to stupify the
travelers to facilitate robbery,snatching and theft. These are mixed with sweet
drinks, confectionaries, jhalmuries, chanachure, beetle leaf and cigarettes.
Common places of using these poisons are railway station, steamer & launch ghat,
bus-stands & terminals, mela and other places of public gathering.
(iii) Accidental poisoning is common in children.
(vii) In most cases injudicious and non-pharmacological use of dhatura seeds by
kabirajs/ Bayddahs/ Hakims in their medicine
Reference:
1.
Rumack BH. “Anticholinergic poisoning: treatment with physostigmine”. Paediatr
1973; 52: 449-451
2.
Sudip et al. “Atropine intoxication from the ingestion and smoking of Jimson weed
(Dutura stramonium)”. Vet Hum Toxicol 1991: 33: 588-589.
85
Chapter -11
Puffer Fish Poisoning
Lesson: 11
Objectives:

Identify puffer fish and classify as
distributions and characters

Describe the chemistry, molecular
pharmacology and toxicology in
relation to puffer fish

Tell the sign and symptom of puffer
fish poisoning

Describe the treatment of puffer fish
poisoning
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Introduction :
Puffer fish poisoning in our country though uncommon is not rare. This fish is consumed
like other fishes everywhere of the world. In Japan, people take this fish as an Epicurean
food, which cost high prices in the market and restaurants and hence the episode of this
poison is much more there. In between 1945-63, Japanese Ministry of Health and Welfare
recorded 1962 Fugu (Puffer) fish poisoning cases of which 1153 cases were fatal. Now,
with the improved control over the preparations and cooking the incidences of mishap
have been remarkably reduced.
In Bangladesh, India and Sril-anka, there have sporadic reports of this poisoning since long
time. But fortunately it is not a popular fish in these countries. It is usually taken by the
lower class people during late Autumn or in Winter.
Description:
a. Distribution: The puffer fish also known as Globe fish, Balloon fish, Blow fish,
Todd fish or Fugu fish is found in sea water, river water even in small water
reservoirs, all over the world.
Though they are world widely distributed, large number of them are found in the
tropical countries. The toxic puffer fish have a prominent specialized exocrine
gland containing poison tetradotoxin.
b. Character: This fish belongs to the family Tetradonitidae. They can swell up
themselves with air or water as their defense mechanism and becomes almost
spherical. They are of various species and all of them are not poisonous.
Fig: Puffer fish
Tetradoxin:
Origin and Occurrence:
Tetrodotoxin (TTX) has been detected from the Fugu Fish and also from a number of
phylogenetically distinct animal species such as star fish, Xanthid crabs, marine shells and
snails, flat worms, Ribbon worms, Horseshoe, in the salivary glands of Australian blue
ringed Octopus, from the skin of frogs. Even from the red calcareous algae and newts.
Biogenesis of tetradotoxin is still not fully understood.
TTX seems to be of importance in (i) Self defense & protective function ofthe animals, (ii)
for their digestive function- as saliva, and- (iii) for immobilization of their prey.
88
a) Chemistry:
TTX structure was elucidated in 1964 and characterized as an
amino-perhydroguinazoline compound with a hamilacto functions having 3
derivatives- tetrodonic acid, 4 epi tetrodotoxin and anhydrotetrodotoxin. TTX is of
amphoteric nature, soluble in acidic water, insoluble in organic solvents and stable at
ambient temperature.
b) Molecular Pharmacology:
TTX binds with the sodium channels, so inward flow of sodium ions through the
channel is blocked leading to inhibition of membrane potentials. Recent data suggests
that the structural dependence of TTX action is of a complex nature.
c) Toxicology:
I. Toxic part: In some species the whole part of the fish is toxic. Usually a) skin, b)
Liver, c) Gonads (ovary, uterus or testis), d) Intestine e) Muscles and f) blood
contains this TTX
II. Sex: Females are more toxic than male; highest being in the ovaries during
reproductive cycle.
Ill. Period: Toxic level is higher during sparming (egging) period (March to June) of
the year.
IV. Nature of the toxin: TTX is one of the most toxic substance known to human
beings. Its strength of toxicity is a) 275 times deadlier than cyannide poison. b) 50
times deadlier than strychnine and curare poison.
V. Fatal period: 6-12 hours, shortest being- 17 minutes
VI. Fatal Dose: Uncertain, depends upon the amount ingested and the season of the
year.
d) Action:
Tetradotoxin is a neurotoxin, which prevents ionic permeability of sodium in the
tissue. It produce hypotension associated with depression of the respiratory center
causing respiratory paralysis and ultimately death due to asphyxia as a result of
respiratory failure. The CNS action probably causes hypothermia and paralysis of both
sensory and motor functions and reversibly blocked by the toxin causing fatality.
Signs and Symptoms:
a) Onset of the poisoning is very rapid occurring within 5-15 minutes of taking food
containing fugu fish.
b) Sign-symptoms and severity depends upon the amount ingested, type of the fish
and season of the year.
c) Peculiar taste sensation, marked salivation, headache and abdominal pain.
d) Nausea- is common but vomiting is uncommon.
e) Patient becomes hypoxic, unable to speak, move in response to stimuli, and may
remain conscious until a very late stage.
f) As cardiovascular manifestations progressive- hypotension, hypothermia,
bradycardia, depressed AV node conductions, arrhythmias and asystole may be
recorded.
g) No tolerance develops.
h) Rapid development of perioral numbness, parasthesia and paralysis of the limbs
and respiratory muscle followed by dyspnoea and respiratory failure and ultimately
death.
89
Management :
There is no specific antidote for TTX, so there is no definite treatment known. Essentially
symptomatic and supportive treatment is done. Respiratory support is mostly given to
prevent respiratory failure.
1 . Removal of unabsorbed poison by gastric lavage by 2% sodi-bi-carb. solution
repeatedly if presented within one hour.
2. Activated charcoal may absorb rest of the poison from the stomach.
3. Artificial respiration with 02 inhalation by mask-in mild cases, but if respiratory
distress persists patient may require direct ventilatory support and sedatives.
4. Purgation and forced diuresis to lessen absorbed poison is not recommended.
5. I.V. infusion of DNS and other electrolytes to maintain body nutrition and electrolyte
balance, and also to prevent hypotension.
6. Neostigmine can dramatically restore transmission. If a large proportion of the receptors
are blocked, the majority of acetylcholine molecules will normally be
encountered, and destroyed by an acetylcholine esterase molecule before reaching a vacant
receptor. Inhibiting acetyl cholinesterase will thus increase the number of acetylcholine
molecules that will find their way to a vacant receptor, and thus increase the endplate
potential so that it reaches the threshold. It also acts on the central and the peripheral
nervous systems, the autonomic motor and sensory nerves. Atropinization and Inj.
Neostigmine has been used for come round from unconsciousness and restoring
neurogenic power both sensory and motor although no evidence based proof is present.
Dose : injections of neostigmine 0.05 ml/kg body weight along with atropine 0.025 ml/kg
body weight six hourly for one day
7. Steroids for life saving measure although contradiction persist.
Reference:
1.Ahasan HAMN, Mamun AA, Rasul CH, Roy PK. Puffer fish poisoning: a clinical
analysis. Pak J Med Sci 2003; 19:29-32.
2. Sims JK, Ostman DC. Puffer fi sh poisoning: Emergency diagnosis and
management of mild human tetrodotoxication. Ann Emerg Med 1986; 9:1094-8.
3. Chowdhury FR, Mamun AA. A fi shy tale. Student BMJ 2004; 12:349-92.
4. Chowdhury F R, Nazmul Ahasan H A M, Mamunur Rashid A K M, Al Mamun A,
Khaliduzzaman S M. Tetrodotoxin poisoning: a clinical analysis, role of neostigmine and
short-term outcome of 53 cases. Singapore Med J 2007; 48 (9) : 830
90
5. Centers for Disease Control and Prevention (CDC). Tetrodotoxin poisoning associated
with eating puffer fi sh transported from Japan-California, 1996. MMWR Morb Mortal
Wkly Rep 1996; 45:389-91.
6. Benzer T. Tetrodotoxin. eMedicine [online] 2001; 6:1-9. Available
at: www.emedicine.com/emerg/topics76.html. Accessed May 17,
2004.
7. Chew SK, Goh CH, Wang KW, Mah PK, Tan BY. Puffer fish
(Tetrodotoxin) poisoning: clinical report and role of anti-cholinesterasedrugs in therapy.
Singapore Med J 1983; 24:168-71.
8. HAM Nazmul Ahsan, AA Mamun, SR Karim, MA BAker, EA Gazi, CS Bala
Paralytic complication of puffer fish(Tetrodotoxin) poisoning. Singapore Med J 2004,
45(2): 73-74
91
Chapter -12
Household products poisoning
Lesson: 12
Objectives:
 Identify household products and
classify as distributions and
characters
 Demonstrate toxicology
 Clinical features
 Manage poisoning cases
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Poisoning with household products is one of the common poisoning in our country.
Although it is commonly accidental, few cases of suicidal attempt also have been seen
with these products. Children between 9 months to 5 years are usually the victim; there are
many cases of adult poisoning with household products.
Some commonly ingested household products:
Bleach

Sodium hypochlorite

Hydrogen peroxide
Cosmetics and toiletries

Cologne

Hair remover containing thioglycolate

Perfume

After shave lotion

Creams & lotions

Nail polish

Nail polish remover
Detergents

Washing up liquid

Fabric conditioner

Soap

Automatic washing / dish washing machine liquid
Disinfectants

Dichlorometaxylenol

Phenol

Cresol
Petroleum distillates

Kerosene

Paint thinner

Paint brush cleaner

Paraffin

Turpentine substitute

Furniture and floor polish
Bleaches, disinfectants and drain cleaners:
Bleaches contain Sodium hypochlorite (upto 10% available Chlorine). Disinfectants
contain dichlorometaxylenol but phenol and cresol may also be present. Drain cleaners
contain Sodium hydroxide.
Phenol, cresol or drain cleaners are corrosives. If consumption is deliberate and of large
volume, these may lead to corrosive effects in alimentary system and also systemic
toxicity,
94
Management: Like corrosive poisoning.
Detergents & disinfectants:
Although details of common ingredients of liquid detergents and toiletries is not known,
the precise contents are of little clinical importance because none causes toxic effect
except nausea, vomiting and diarrhoea.
Management:
1. Gastric lavage, emesis or GI irrigation is unnecessary
2. No specific treatment is available
3. Symptomatic measures are not often required
4. Observation and support are the main theme of management.
Detergents powder, sterilizing tablets, denture cleaning tablets etc contain ingredients
which have corrosive effects in alimentary system and also on mucosal surface.
Talcum powder is occasionally inhaled by children which may cause severe pulmonary
oedema and death.
Nail polish and nail polish remover contain solvents including acetone. Acetone can cause
acidosis, coma and irritate mucous membrane. But serious toxicity is rare.
Management:
1. No specific antidote is available
2. Supportive treatment as that for corrosive poisoning.
Petroleum distillates:
Paraffin, kerosene and white spirit (Turpentine substitute) are the most common causes of
poisoning with household products. In most cases ingestion is less and toxicity is low. If
large quantity is ingested, then:

Nausea, vomiting, diarrhoea.

CNS excitation followed by impaired consciousness.

Aspiration into respiratory tracts resulting in haemorragic pneumonitis, respiratory
distress.

Cyanosis, respiratory failure.

Convulsion.

Pneumatocele.

Intravascular haemolysis.

Deffating & inflammatory change in skin if prolong contact.
Management:
1. Most cases require no treatment
2. Antibiotics in case of secondary bacterial pneumonia
3. Supportive measures.
Notes:
Emesis and lavage are contraindicated
Gut decontamination have no proven value
Activated charcoal is of no value
Corticosteroids and antibiotics in lupoid pneumonia is of no value
95
Disc batteries:
Batteries may be mercury, alkaline manganese or silver cell. They are easily available and
often swallowed by children.
Hazards:

Batteries larger than 20 mm may stick in oesophagus causing obstruction. It can
cause fever, dysphagia, vomiting and anorexia.

Batteries may break and release their contents.

Rarely toxic amount can be absorbed. Local corrosive effects on gut wall with
subsequent perforation is due to leakage of ingredients and from local electrical
discharge.

Mercury batteries if opened in the gastrointestinal tract can lead to systemic
absorption of mercury.
Management:
Perform chest and abdominal X rays to locate the battery.
(a)
If stuck in oesophagus or there are signs of separation of cells, endoscopic removal
with or without use of magnet.
(b)
If the battery is in the stomach observe for fever, vomiting, abdominal pain and
tarry stool. If these symptoms appear or the battery is still in the stomach (shown
by X-ray) after 24hours, surgical removal may be necessary. In most cases the
material travels through gut in 48 hrs without any harmful effects. But it may also
take one week.
(c)
Radiology is of helps to identify the disintegration of batteries. In case of
disintegration, it should be removed.
(d)
Metoclopramide and laxative are of doubtful value. Alkalis may even be harmful.
96
Lesson: 13
Paracetamol poisoning
Lesson: 13
Objectives:
 Identify the use and abuse of
Paracetamol
 Describe the clinical features
 Tell the management of poisoning
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Introduction:
Paracetamol is the most widely used over-the-counter analgesic/ antipyretic
pharmaceutical. Paracetamol poisoning is the commonest reason for acute liver failure
requiring transplantation in the United Kingdom. A single overdose of more than 12 g (24
tablets) or 150 mg/kg body weight can be potentially fatal. In children, hepatotoxicity
should be anticipated with doses exceeding 125 mg/kg body weight.
Patients with following conditions have a higher risk of paracetamol induced liver damage.

Malnutrition and eating disorders

Chronic alcohol abuse

Recent or ongoing viral illness

Use of enzyme inducing drugs (e.g. Carbamazapine, phenytoin, phenobarbitone)

Cystic fibrosis

HIV infection or NDS
Clinical Features:
Clinical features of paracetamol toxicity can be divided into four distinct phases.
Symptoms range from minor gastrointestinal irritation to coma and death. However, the
majority of acute overdose victims remain relatively asymptomatic.
Phase- I (0-24 hours):
During the first 24 hours, the patient may be asymptomatic, or features of gastrointestinal
irritation predominate with nausea, vomiting and abdominal pain. Rarely, ingestion of
more than 15 gm in adults and more than 10 gm in children can result in metabolic
acidosis within 4 hours of ingestion. Cardiac effects such as arrhythmias or bradycardia
may develop. Biochemical evidence of liver damage is not detectable.
Phase- II (24-72 hours):
After a latent period of 12 to 48 hours, hepatotoxicity develops with elevation of hepatic
enzymes, prothrombin time, and bilirubin. Severe liver damage is indicated if the peak
plasma alanine aminotransferase and aspartate aminotransferase activity exceed 1000 IU/1.
There may be right upper quadrant abdominal pain. Patient may be otherwise
asymptomatic.
Phase- III (72-96 hours):
Hepatic necrosis continues resulting in bleeding manifestations, portal hypertension,
hepatic encephalopathy and elevated bilirubin levels. Thrombocytopenia, hypoglycaernia,
disseminated intravascular coagulation, hypokalaemia, pancreatitis and myocarditis may
be observed. Oliguric renal failure may develop due to renal tubular necrosis, usually
associated with hepatoceilular necrosis. Patient may develop coma. Death is due to hepatic
failure.
98
Phase- IV (96 hours-2 weeks):
Hepatic failure and death may occur, or there may be complete resolution of hepatic
damage and recovery.
Management
Management depends on the time interval since ingestion and the plasma paracetamol
levels. In Bangladesh, there is no facility to determine the serum paracetamol levels so for.
On admission, perform liver function tests, prothrombin time, full blood count, urine
analysis, renal function tests, blood glucose and serum electrolytes. Repeat these tests
daily. Perform gastric lavage in adults. Give syrup of ipecac to induce emesis in children.
Give activated charcoal 50 to 100 g in 200 ml of water.
N-Acetylcysteine (NAC) and Methionine are the antidotes which protect the liver up to 12
hours of an overdose of paracetamol. Methionine is less effective. Now there is good
evidence that NAC is effective up to 24 hours even if there is hepatic damage and that
repeated NAC infusions produce significantly greater survival and fewer neurological and
cardiovascular complications.
Dosage for NAC infusion (IV)
Adult: 150 mg/kg IV in 200 ml of 5% dextrose over 15 minutes, followed by 50 mg/kg IV
in 500 ml dextrose over 4 hours, followed by 100 mg/kg IV in 1000 ml 5% dextrose over
16 hours.
Children (less than 20 kg): 150 mg/kg IV in 3 ml/kg of 5% dextrose over 15 minutes,
followed by 50 mg/kg IV in 7 ml/kg of 5% dextrose over 4 hours, followed by 100 mg/kg
IV in 14 ml/kg of 5% dextrose over 16 hours.
If for any reason dextrose is unsuitable, 0.9% sodium chloride solution may be substituted.
With established hepatotoxicity, continue NAC treatment 50 mg/kg in 500 ml of 5%
dextrose over 8 hours. Repeat until prothrombin time and liver enzymes begin to return to
normal.
Patients may develop rashes, bronchospasm, angioedema and hypotension following NAC.
Discontinue the infusion of NAC for 1 to 2 hours and give an antihistamine such as
chlorpheniramine.
Dosage for oral NAC: If NAC IV preparation is not available, give 140 mg/kg of oral
NAC as a loading dose, followed 4 hours later with 70 mg/kg given every four hours for
an additional 17 doses.
For patients weighing up to 20 kg, dilute each ml of NAC with 3 ml of fruit or soft drink.
If the weight is more than 20 kg, dilute with enough soft drink or juice to make a 5%
solution.
Diluted solutions should be freshly prepared and used within 1 hour. Any dose vomited
within one hour of administration should be repeated.
99
Dosage of methionine (oral):
If NAC is not available, give methionine 2.5 g orally, followed by 3 doses of 2.5 g, 4
hourly. The total dose is 10 g.
Paediatric dose (< 20 kg): Methionine 1 g orally, followed by 3 doses of 1 g, 4 hourly. The
total dose is 4 g.
(Methionine is not recommended to be started more than 10-12 hours after the overdose,
or if there is established liver injury.)
Recommendations of antidote use:
Use methionine if,

Patient is admitted within 8 hours of single overdose

Admitted after 8 hours of overdose and on admission
patient is asymptomatic (no vomiting and no right
hypochondrial tenderness). In Such patients liver
enzymes (SGOT and SGPT) should be measured on
admission and if they are normal, methionine can be
continued. If enzymes levels are elevated antidote should
be changed to NAC
Use intravenous NAC if,

A patient presents more than 8 hours after single
overdose and is symptomatic (vomiting and right
hypochondriac tenderness)

A high risk patient has ingested more than 75 mg/kg

A person has ingested a single overdose of more than
150mg/kg or more than 12 g (24 tablets)

A person has ingested more than 7.5 - 10 g/day over a
short period of time.

A child has ingested more than 90 mg/kg/day.
Maintain a fluid balance chart. Correct hypoglycemia.
The prothrombin time and plasma creatinine should be determined on completion of the
treatment before discharge.
If a patient presents 8 to 15 hours after ingestion, urgent action is required because the
efficacy of antidotes declines progressively from 8 hours after ingestion. It is
recommended that NAC should be given to patients admitted 16 to 50 hours after
ingestion, if they are considered to be at risk of developing liver failure.
Once commenced, NAC treatment should be completed unless there is anaphylaxis. If
NAC was started for progressive liver dysfunction, it should be continued until the
prothrombin time begins to fall.
100
At the end of the NAC infusion, a blood sample should be taken for determination of
prothrombin time and plasma creatinine levels. If these are normal and the patient is
asymptomatic, risk of severe liver damage is negligible. Patients who are symptomatic, or
in whom prothrombin time and/or plasma creatinine levels are abnormal, further
monitoring is required.
Haemodialysis is useful in renal failure secondary to hepatic failure.
Vitamin K1 should be given if the prothrombin time is increased. Fresh frozen plasma and
clotting factors are indicated for active bleeding and severe coagulation abnormalities.
Fulminant hepatic failure should be managed as follows:

Monitor liver function, renal function, urine output and the grade of
encephalopathy. Give Vitamin K1 (11 mg/kg) if the prothrombin time is elevated.

For cerebral oedema, give mannitol IV (0.6-1 g/kg) as a 20% solution by rapid
bolus injection over 15 minutes. Mannitol may be repeated twice, over next 4-8
hours if needed (not at fixed dose intervals) ensuring that the urine output is good.

Give broad spectrum antibiotics IV.

Give proton pump inhibitor to prevent gastrointestinal haemorrhage.

Give fresh frozen plasma (10 ml/kg every 6 hours), if active bleeding occurs.

Give NAC if not already given and/or continue with 50 mg/kg in 500 ml of 5%
dextrose over 8 hours. Repeat until recovery.

Administer 10% dextrose IV, with added potassium at a minimum rate of 3
mEq/kg/24 hours (usually 3-6 mEq/kg/24 hours) if there is no renal failure.
Monitor glucose levels four hourly and prevent hypoglycaemia.

If renal failure ensues, commence dialysis/haemofiltration. Frusemide infusion of
10 mg/hour may be tried.
There is increased survival following liver transplantation in patients with paracetamol
induced fulminant hepatic failure. It is necessary to define early prognostic indicators in
these patients. The factors which may indicate patients with a probable fatal outcome are:

Grade III or IV encephalopathy

Acidosis (PH < 7.3)

Prothrombin time more than 160 seconds

Serum creatinine more than 3.4 mg/dl
Liver transplantation is the treatment for patients fulfilling the above criteria. Patients who
recover from liver damage should not consume alcohol for at least three months.
Reference:
1.Buckley NA, Whyte IM, O’Connell DL, et al.c Activated charcoal reduces the need for
N-acetylcysteine treatment after acetaminophen(paracetamol) overdose. J Toxicol Clin
Toxicolv1999;37:753–757.
2. Prescott LF, Illingworth RN, Critchley JAJH, et al. Intravenous N-acetylcysteine: the
treatment of choice for paracetamol poisoning. BMJ 1979;2:1097–1100.
101
3. Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics
1975;55:871–876.
4.Perry HE, Shannon MW. Efficacy of oral versus intravenous N-acetylcysteine in
acetaminophen overdose: results of an open-label, clinical trial. J Pediatr
1998;132:149–152.
5. Dougherty T, Greene T, Roberts JR. Acetaminophen overdose: comparison between
continuous and intermittent intravenous N-acetylcysteine 48-hour protocols. Ann Emerg
Med 2000;36:S83.
6. Woo OF, Mueller PD, Olson KR, et al. Shorter duration of oral N-acetylcysteine
therapy for acute acetaminophen overdose. Ann Emerg Med ,2000;35:363–368
7. Hamlyn AN, Lesna M, Record CO, et al. Methionine and cysteamine in paracetamol
(acetaminophen) overdose, prospective controlled trial of early therapy. J Int Med Res
1981;9:226–231.
8. Alsalim W, Fadel M. Oral methionine compared with intravenous n-acetyl cysteine for
paracetamol overdose. Emerg Med J 2003;20:366–367.
102
Chapter - 14
Approach to Diagnosis and Management of Snakebite
Duration: 1hour and 30 minutes
Lesson: 14
Objectives:
 Tell about venomous snakebite
 Record a complete history from the patient /
attendant
 Conduct a physical examination of the patient
looking for significant signs of envenoming and
diagnosis of the snakebite patient
 Provide appropriate first aid and urgent treatment
 Administrate the Antivenom
 Manage the antivenom reactions
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Introduction:
What is venomous snakebite?
A bite by a venomous snake which produces specific symptoms or a syndrome is
considered as a venomous snake bite. It is important to note that a bite by venomous snake
may not and do not always produce features of envenoming. It has been found that about
50% of bites by Russell's vipers, 30% of bites by cobras and 5-10 % of bites by saw-scaled
vipers do not result in any symptoms or signs of envenoming.
A bite by a non venomous snake does not produce the specific features due to venom. But
the care giver should be cautious about the effect of various commonly practiced local
treatment (e.g. by'Ozhas') of snake bite.
A victim may develop some features due to anxiety or apprehension in case of bite by a
venomous as well as non venomous snake.
Medically important snakes of Bangladesh (Pics at the end of this chapter)
The medically most important venomous snake species in Bangladesh are three species of
krait (Bungarus walli, Bungarus caeruleus, Bungarus niger), two species of cobra (Naja
kaouthia, Naja naja), and green pitvipers (Cryptelytrops spp.). Russell's Viper (Daboia
russelii) appears to be rare and its distribution patchy and/or restricted to western and
northern parts of the country. There has been no recent report of proven case of Russell's
viper envenoming in Bangladesh. Several other species of dangerously venomous snakes
exist in Bangladesh but have not been involved in proven cases of envenoming in recent
years. Krait and cobra envenoming is associated with high mortality; cobra envenoming
frequently causes permanent disability; green pitviper envenoming often causes significant
morbidity but is rarely fatal.
Taking a relevant clinical history:
 Site of bite, circumstance of bite, time of bite, how did it happen?
Site
• Face and head-Green snake
• Limbs-Cobra
• Any site-Krait
• Forearm-Sea snake
Time of bite
• Night time bite especially in krait

Non-specific symptoms: Headache, nausea, vomiting, abdominal pain, loss of
consciousness, difficulty in vision, convulsions.

Neurological symptoms: Muscle paralysis, difficulty in moving jaw, tongue, eye,
heaviness of eye lids (ptosis), weakness of neck muscle (Broken neck sign) difficulty
in swallowing, dribbling of saliva, nasal regurgitation, nasal voice, difficulty in
respiration, extreme generalized weakness.
105

Haematological symptoms: Spontaneous bleeding from gum, vomiting of blood,
haemoptysis, haematuria, persistent bleeding from bite site, venepuncture site and
inflicted wound if any.

Others: Severe muscle pain, dark coloured urine, scanty urine volume, collapse
(cardiovascular).

Any important concomitant medical problem: History of allergy, bronchial asthma,
kidney, heart disease, bleeding disorders, neurological diseases, limb swelling etc.

In female: whether the victim is pregnant or not, whether the victim is menstruating or
not.
 History of Pre hospital treatment:
For example
 Home treatment.
 Treatment from traditional healers ('ozha').
 Application of tourniquet.
 History of immunization against tetanus.
 Treatment by initial attending physician
The physical examination
1) Rapid clinical assessment, especially monitoring of vital signs (Pulse, Respiration,
Temperature, Blood Pressure).
2) Systemic signs of envenoming: chronology of onset and progression of signs.
a. Neurotoxic sign:
Ptosis (partial of complete) usually symmetrical and progressive
Diplopia, external ophthalmoplegia
Loss of gag reflex / palatal palsy (Bulbar palsy)
Dysphonia / Nasal voice
Facial paralysis,
Inability to open the mouth, protrude the tongue
Paralysis of chest muscles and diaphragm (shallow breathing)
'Broken neck sign', weak grip, diminished tendon reflexes
b. Signs of haematological abnormalities:
Persistent bleeding from bite site,venepuncture site and or inflicted wound if any,
Multiple bruise or large blood collection, haemorrhagic blisters, bleeding from
gingival sulci, haemoptysis, haematemesis, haematuria, epistaxis.
c. Signs of Renal failure:
scanty or no urine output, dark coloured urine Clinical uraemic syndrome : Nausea,
vomiting, hiccups, fetor, drowsiness, coma, flapping tremor, muscle twitching,
convulsions, pericardial friction rub, signs of fluid overload.
106
d. Signs of myotoxicity:
Muscle tenderness, weakness, respiratory failure, black urine, renal failure
e. Signs of local envenomation
Swelling, tenderness, bleeding, ulceration, necrosis, local lymph node enlargement
Identification of snake:
By description or by model, photography, brought snake, preserved specimen (10%
formalin fixed)
Laboratory Investigations (depending on clinical features)

Coagulation tests - 20 min whole blood clotting test

ECG

Complete blood count

Blood grouping & Rh typing

Blood urea, S. creatinine

Urine R/E

Serum CPK

Immuno diagnosis (by ELISA).
20 minutes whole blood clotting test (20WBCT):

Place a few ml of freshly sampled venous blood in a small glass tube

Leave undisturbed in erect position for 20 minutes at ambient temperature Tip the
tube once

If the blood is still liquid (unclotted) and runs out, the patient has
hypofibrinogenaernia "incoagulable blood" as a result of venom induced
consumption coagulopathy

In perspective of Bangladesh, incoagulable blood is diagnostic of a viper bite and
rules out an elapid bite

Warning: If the tube used for the test is not made of ordinary glass, or if it has been
used before and cleaned with detergent, its wall may not stimulate clotting of the
blood sample in the usual way and test will be invalid. If there is any doubt repeat
the test in duplicate, including a "Control" (blood from a healthy person)
Local swelling and tissue damage:
First sign of envenornation (Exceptions: kraits, sometime with cobras) Blisters,
necrosis
Other General Examination:
Physical examination Respiratory system, Cardiovascular system, Nervous system,
Alimentary system, Locomotor system
107
Syndromic Approach:
Although there may be considerable overlap of clinical features caused by venoms
of different species of snake, a "Syndromic approach" may be useful especially
when the snake has not been identified and only monospecific antivenom is
available.
Syndrome - 1
Local envenoming (swelling of extremities etc.) with bleeding / clotting disturbances =
viperidae (all species) Whether local swelling is due to snake bite or due to bandage has to
be mentioned
Syndrome - 2
Local envenoming (swelling etc) with bleeding / clotting disturbances, shock or renal
failure with ptosis, external ophthalmoplegia, facial paralysis etc. and dark brown urine =
Russell's viper
Syndrome - 3
Local envenoming (swelling etc.) with paralysis with no sign of bleeding or clotting
disturbances = Cobra or King cobra.
Syndrome - 4
Paralysis with no local envenoming
Bite on land while sleeping = Krait
Bite in the sea = Sea Snake
Syndrome - 5
Paralysis with dark brown colour urine and renal failure, no local envenoming, no bleeding
or clotting disturbances, severe muscle pain. Bite in the sea (no bleeding/ clotting
disturbances) = Sea snake
The Management of Snake Bites:
First aid treatment:
When a patient comes with a history of snake bite or when snake bite is suspected,
immediate treatment is to be started. The first aid is to provide to the victim of snake bite
as soon as possible after the bite before reaching any health facilities by the victim himself
or herself or by a someone else who is present at the vicinity.
Recommended first aid methods

Reassurance: Reassure the victim who may be very anxious.

Immobilize the bitten limb with a splint or sling as practiced in fracture of long
bone.

If the bite is in lower limb: do not walk.

If the bite is in upper limb: do not move the limb.
108

Ideal is to provide pressure immobilization, which is especially helpful for
venomous cobra and krait bite. This should not be used for viper bite including
Green snake.
Pressure immobilization method:
We can give pressure by simple, crepe bandage or by any long strips of cloths (like
Gamchha). The bandage is wrapped firmly around the entire bitten limbs, starting distally
around the fingers or toes and moving proximally, to include a rigid splint. The bandage is
bound as tightly as for a sprained ankle, but not so tightly that the peripheral pulse (Radial,
posterior tibial, dorsalis pedis) is occluded or that a finger cannot easily be slipped
between its layers.
Ideally, compression bandages should not be released until the patient is under medical
care in hospital, resuscitation facilities are available and antivenom treatment has been
started.
Some harmful traditional treatments in our country

Cauterization by using chemicals like carbolic acid.

Application of multiple tight arterial tourniquet.

Shedding of profuse blood by multiple incisions over and around the bite site.

Incision and suction of bite site by mouth or by chick.

Application of different herbal paste or even cow dung and mud.

Ingestion of oil, ghee, pepper, crude herbal product etc. to induce vomiting.

Application of stones, seeds, saliva (in an encircled fashion) over bite site.

And lot of other
Disadvantage of traditional treatment:
From scientific point of view, these traditional methods are simply waste of time. More
over, they are harmful. The patient may develop severe infection, bleeding, gangrene.
Sometimes they can damage vein, artery, and muscle of the limb; even tetanus may occur.
Sometimes they may cause more harm than the snake venom itself. Even one may not get
expected result of scientific treatment due to usual delay pursuing traditional treatment.

Quick transfer of the victim to the nearest health facility (Community clinic / THC/
District Hospital / Medical College Hospital)

Do not waste time for seeking useless some times harmful treatment provided by
traditional healers ('Ohzas').

Do not provide anything by mouth if the victim has difficulty in swallowing, has
vomiting or nasal voice.
Treatment in the health facility:
109
I) Rapid clinical assessment and resuscitation:
Airway: Maintain clear airway by proper examination and suction if necessary
Breathing: Observe the chest movement, respiratory rate, and cyanosis, if
necessary provide immediate support by mouth-to-mouth breathing, subsequently
by Ambo bag. If facility is available patient should be intubated and should be put
on mechanical ventilator or manual breathing by Ambo bag.
Circulation: Assess pulse, blood pressure. Support by intravenous access and fluid
(preferably normal saline)
II) Detailed clinical assessment:
a. History:
Key points:
1.
Circumstances of the bite
2.
Site of bite
3.
Time of bite
4.
Progressive symptoms and signs
5.
Description of the snake if seen, or if the snake is killed, whether it is
brought or if not request the party to bring it if left at the bite site.
Indication of severe envenoming:
Local:
• Rapid extension of local swelling
• Blistering, necrosis
Neurological:
• Heaviness of the eyelid with or with out blurred vision (paralysis of eye ball
muscle)
• Nasal voice
• Difficulty in swallowing
• Difficulty in breathing
• Difficulty in opening of the mouth, protruding the tongue
• Weakness of neck muscles ('broken neck sign')
Haematological:
• Early spontaneous systemic bleeding (gum, gingival sulci, epistaxis,
ecchymoses)
• Subconjunctival haemorrhage
Others:
• Passage of dark or brown coloured urine, oliguria
• Vomiting
• Collapse
Approach to Identification of species
110
1. Brought snake, live or dead; or definitive description; or by photograph
2. 20 minute whole blood clotting test (20 WBCT). In Bangladesh,
incoagulable blood is diagnostic of a viper bite.
3. Syndromic approach.
N. B. Do not attempt to kill the snake, as this may be dangerous. Do not handle the
snake with bare hands, as even a severed head can bite.
III) Treatment:
1. Antibiotic
2. Tetanus prophylaxis
3. Antivenom: (At present only polyvalent antivenom is available in our country)
4. Additional treatment
Indications / Criteria for using Polyvalent antivenom:
1 Neurotoxic signs:
Ptosis
External ophthalmoplegia
Broken neck sign
Nasal voice
Respiratory difficulty, etc.
2. Rapid extension of local swelling (more than half of bitten limb) not due to Green
snake bite or tight touriquet.
3. Acute renal failure not due to sea snake bite.
4. Cardiovascular abnormalities.
5. Bleeding abnormalities in russel viper bite
6. Haemoglobinuria / Myoglobinuria not due to sea snakes.
Poly valent antivenom:
In our country, now polyvalent antivenorn is only available in Iyophilized powder form.
Each vial contain 10 mg of antivenom, which is effective against systemic envenoming by
Cobra, Krait, Russell's Viper and Saw scaled viper only (there is no evidence of Saw
scaled viper in Bangladesh). So this type of antivenom should not be used in bites by
Green snake, Sea snakes and identified nonvenomous snake.
Indications of monovalent antivenom:
The snake is definitely identified with signs, symptoms of envenoming.
Anti snake venom therapy:
Dose: Each dose consists of 10 vials of polyvalent antivenom irrespective of age and sex
of the victim.
Time and administration:
111
Each vial is diluted with 10ml. of distilled water. 10 such vials (100 ml) is further diluted
or mixed with 100 ml of fluid (Dextrose water or saline). Then it is administered as
intravenous infusion within 40-60 min (60-70 drops/min).
Observation and monitoring:
Continuous observation and frequent monitoring of vital signs should be ensured during
antivenom therapy and few hours after its completion. Careful clinical assessment for
appearance of signs and symptoms of antivenom reaction should be performed.
Antivenom reaction: Three types of A/V reaction can occur
1. Early anaphylaxis:
Usually develops within 10 -180 min of starting of antivenom. Common features are
itching, which may be intense, urticaria, fever, angio- oedema, dyspnoea due to
bronchospasm, laryngeal oedema, hypotension etc. Other features are abdominal pain,
vomiting, diarrhoea, etc.
Treatment of anaphylaxis:
A. Temporary suspension of AV administration
B. Adrenaline: 1: 1000 solution
For adults: 0.5 ml (500 μg) IM
For children: (0.01 mg/kg.) IM
6- 11 years: 0.25 ml (250 μg) IM
2-5 years: 0.125ml (125 μg) IM
Indications of adrenaline injection:
Should be given at the very first sign of a reaction even when only a few spots of
urticaria have appeared, or at the start of itching, tachycardia, or restlessness. Dose
can be repeated every 5-10 min interval if the patient's condition is deteriorating.
C. Antihistamine (Chlorpheniramin maleate)
Adult = 10 mg slow IV after dilution
Child = 0.2 mg/kg slow IV after dilution
D. Hydrocortisone: 100 mg IV for adults, 2mg/kg for children.
E. Ranitidine (H2 blockers) to be given IV slowly. Adults = 50 mg, Children= 1
mg/kg
2. Pyrogenic reaction:
Usually develops 1-2 hrs after treatment. Features include chills rigors, fever, fall of BP;
febrile convulsion may develop in children.
Treatment of pyrogenic reaction: Tepid Sponging, fanning.
Anti pyretic like Paracetamol suppository, IV fluid.
112
3. Late reaction (Serum sickness type):
May develop 1- 12 (mean 7) days after treatment. Features include, fever, itching,
recurrent urticaria, arthralgia, myalgia, lymphadenopathy, proteinuria etc.
Treatment of late reaction: Antihistamine, Prednisolone (when no response to
antihistamine)
N. B. Routine skin sensitivity test for AV before starting treatment is not recommended.
When the victim has history of Asthma, COPD or when the victim is a pregnant lady,
adrenaline prophylaxis (subcutaneously half the dose used for treatment) should be given
before giving anti snake venom.
Additional treatment:
1. Neostigmine - Atropine combination:
Indicated for neurotoxic features only
Dose: Inj Atropine 15 μg/kg IV followed by Inj Neostigmine 50 -100 μg/kg SC; every 4
hourly, until neurotoxic features improve
2. Respiratory support:
In case of neurotoxic envenoming with bulbar and respiratory paralysis, antivenom alone
cannot be relied upon to prevent early death from asphyxiation. Artificial ventilation is
essential in such cases.
3. Fresh blood transfusion: For patients with coagulopathy.
Criteria for repeating the initial dose of antivenom:
Persisting or deteriorating signs of systemic envenoming e.g.
a) If no improvement or deterioration of neurotoxic features (Cobra or
Krait) 1-2 hours after completion of antivenom.
b) Persistence or recurrence of blood incoagulability after 6 hours of
antivenom treatment
Drugs not recommended:
1. Antihistamine except for antivenom reaction
2. Corticosteroid except for antivenom reaction
3. Sedative
4. Anti fibrinolytic agent
5. Heparin
6. Traditional medicines (from Ohza)
113
Treatment of bitten part:

Elevation of limb with rest

Simple washing with antiseptic solution

Broad-spectrum antibiotic (esp. when there is features of contamination, multiple
incisions etc.)

In case of local necrosis and gangrene:
o
Broad spectrum antibiotic
o
Surgical debridement and split thickness skin grafting is indicated but
decision should be made with caution.
Rehabilitation:
Long term consequence of snake bite like contracture and disability can be avoided by
maintaining the affected limb in functioning position initially and restoration of normal
function by physiotherapy.
Conservative treatment when no antivenom is available:
This may be the situation in many parts of Bangladesh where antivenom is not supplied or
available.
The following conservative measures are suggested:
a) Assisted ventilation in cases of neurotoxic envenoming with respiratory paralysis.
It has been proved effective and has been followed by complete recovery, even
after being maintained for long period. Manual ventilation by anesthetics bag
(Ambo bag) by doctor, students, nurses or even by relatives can be maintained.
Endotracheal Intubation followed by ventilation (where available) is more helpful.
Anticholinesterase (neostigmine)-Atropine combination should always be tried in
these situations.
b) In case of haemostatic abnormalities
1) Strict bed rest to avoid even minor trauma
2) IM injection must be avoided.
3) Fresh whole blood transfusion should be given.
Reference:
1. WHO progress in the characterization of venoms and standardization of antivenoms,
1981,Geneva: World Health Organization.
2. Khan M A R. Sareesrip Prani. In: Bangladesher Bannya Prani. Dhaka: Bangla
Academy,1987: 42-168.
3. Wuster W. Thorpe R S. Asiatic cobras: Experiantia, 1991:47: 205-209.
114
4. Faiz M A. Raman M R, Das J C, Neurotoxicity and tissue necrosis following bite by
cobra (Naja). Abstract, Dhaka Congress, 1994.
5. Warrell D A. Snake venoms in science and clinical medicine. Russell’s viper: biology,
venom and treatment of bites. Tr R Soc Trop Hyg, 1989: 83: 732-740.
6. Minton S A. Neurotoxic snake envenoming. Sem Neurol, 1990: 10: 52-61.
7. Hug F, Islam M A ET AL, Epidemiology of snake bite in Bangladesh. Bangladesh J
Zool,1995 : 23 : 61-64.
8. Warrell D A. Clinical toxicology of snake bite in Asia. In: Handbook of clinical
toxicology of animal venoms and poisons. Jung Meier and Julian White ed, 1995: 536
9. Teakston R D G et al, Envenoming by the common Krait and Sri Lankan cobra ( Naja
naja): Efficacy and complications of therapy with Haffkine antivenom. Trans R Soc
Trop Med Hyg,1990 : 84/21: 301-389 .
10. Sutherland SK. Antivenom use in Australia: premedication, adverse reactions and the
use of venom detection kits. Medical journal of Australia 1992; 157: 734-35.
11. Manuals on Guidelines of Snake Bite Management and Treatment in Bangladesh
12. Sutherland. S .K. Acute untoward reactions to antivenoms, Med. J. Aust,1997, 2; 841
115
Important venomous snakes of Bangladesh
Fig 1 (A): Common Cobra -Monocellete cobra

Fig 1 (B): Common Cobra- Binocellete cobra
(Naja kaouthia)- Copy right Prof MA Faiz

(Naja naja) Copy right Dr. T S N Murthy
Fig 2: King Cobra (Opiophagus hannah
Copy right Dr. T SN Murthi
B. Walli B. Caeruleus
Fig 3: Black krait (Bungarus wali) and Common Krait (Bungarus caeruleus)
Copyright: Ulrich Kuch
Fig 4: Bungarus niger

Fig 5: Bungurus lividus

Fig 6 (A & B): Russell's viper (Daboia russelii)
Copy right Professor D A Warrell
A B
Fig 7 (A & B): Green snake (Cryptelytrops spp
Copy right: Professor M A Faiz)
Fig 8 (A & B): Sea snake (Hydrophidae spp
Copy right: Professor D A Warrell)
Key Features of Poisoning
Fig 9: Ptosis (Neurotoxic snake bite

Fig 10: Localized envenoming

(angioedema)
Fig 11: "Broken neck" sign
(Copy right: Professor M A Faiz)
A B
Fig 12 (A & B): Hemorrhagic blister (Features of local envenoming); copy right: Professor M A Faiz
Fig. 13: Technique of Pressure immobilization
ALGORITHM 1: Management of snake bite in hospital (Medical College Hospital / District Hospital /
 Quick assessment
Thana Health Complex)
 Support vital signs
Patients with
 Ensure appropriate initial treatment
history of snake bite
Snake identified
Brought specimen or seen definitely or
identified by photograph
No Yes
Signs & symptoms of

Snake is venomous Snake is non-
envenoming
venomous
 Reassure
No Yes Signs met criteria for

 Tetanus prophylaxis
Polyvalent anti
 Discharge
venom treatment
Observe in
 Polyvalent
hospital for 24
antivenom treatment
hours
 Additional treatment
 Monovalent
anti-venom
Signs and
treatment
symptoms of
 Additional
Signs met
treatment
envenoming
Yes
criteria for mono
(Green-snake,Sea-
appear
valent antivenom
snake)
treatment
No
Check response
 Reassure
 Tetanus
Signs of persisting systemic envenoming
prophylaxis
 Discharge
No Yes
Observe and
Repeat
continue other
antivenom
treatment
treatment
Chapter–15
Deliberate self-harm poisoning
Duration: 1hour
Lesson: 15
Objectives:
 Tell the definition of Deliberate self harm
poisoning
 Assess the psychological status before
and after the act
 Provide psychological support during
recovery stage
 Assess the further risk of DSH poisoning
 Manage the psychiatric care
 Describe the flow chart of DSH
assessment
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Definition of Deliberate Self Harm ( by poisoning):
Self poisoning are named differently- Attempted suicide / Para suicide / Deliberate self
harm.
** Episodes of intentional self-harm that may or may not have motivated by a disease to
end life.
‘Non fatal act in which an individual deliberately causes self injury / ingest a
substance in excess of any prescribed or generally recognized dosage.’
The intent does not specify the suicidal intent.
Differentiation between suicide and DSH is not absolute and often it is difficult to do
so.
There is important overlap between the two.
Why to do psychiatric assessment in a poisoning case?
In all poisoning cases (except homicidal or accidental poisoning) who are trying to die by
their own have some emotional component in back ground. It is seen in different studies
that among self-poisoning or deliberate self harm group of patients 5 -15% needs
psychiatric admission and more large number need psychological support and counseling.
In follow up studies it is also evident that psychological assessment can prevent further self-
poisoning and consequent suicide rate. Suicidal rate in subsequent 12 month is 100 times
more common than general population in deliberate self harm patients. Some patients of
self-poisoning has associated psychiatric disorders and personality disorders. Among the
psychiatric problems depression is most common followed by drug abuse, alcohol
dependence and schizophrenia. Impulse control disorders are again an important reason of
self-poisoning, where the person has very little control on self and poor skill in managing
different life stress & strain. No self-poisoning case should be taken lightly as some non
fatal cases may have a dangerous intent in future.
Deliberate self harm:
a) Self poisoning:
In UK 98% DSH referred to general hospital involve drug overdose like
Paracetamol/Aspirin (thinking them as non fatal). Forty percent of them take alcohol 6hr
before act. In our country most of the DSH patients take pesticides, sleeping pills and often
arsenic.
b) Self Injury:
Violent self injury is commonly done by male and in developed countries it includes
laceration in forearm-wrist, jumping from height, in front of train, motor vehicle, shooting
and drowning.
Personality problems:
Deliberate self-harm by poisoning and injury are common in people with low
selfesteem/who are impulsive in nature / aggressive in behavior, also in people who are of
unstable mood. Most of the persons of these disorders have difficulties in interpersonal
relationship.

They have high alcohol and drug abuse habit.

There is a strong association between DSH and childhood sexual abuse.

The problem of DSH increasing gradually in all cultures including ours.
Age & sex variation:
More common in younger people, two times more common in females (highest in divorced
woman), low socioeconomic and rural background. Rare below 12 years.
Causes of DSH:
1) Precipitating factors:
Most of the patients of deliberate self poisoning experiences 4 times more life stress in last
6 months of the happening. Usually it is seen to be related with immediate family members
like.
* quarrel with spouse,
girl/boy friends,
Other relatives
separation/ rejection by boy/ girl friends,
failure in love affairs,
failure in examination or
failure to achieve the expected result,
Illness of a family member,
recent personal physical illness,
loss in business
2) Predisposing factors:
Familial and developmental factors are mostly held responsible like
i) Early parental loss through bereavement,
ii) History of parental neglect / abuse.
iii) Personality problems like poor skill in solving personal problem/ planning for
future/ hopelessness / impulsiveness.
In men- Unemployed in recent years brings a remarkable merit in causing self poisoning
probably through financial difficulties in maintaining living hood. In women: DSH is more
seen in unemployed in last 1 yr. Poor physical health-epilepsy and cancer.
Psychiatric disorders:
Depression is more common in hospitalized DSH patients. In hospitalized suicidal
attempted patients (either by poisoning or self injury) high rate of depression is seen at the
time of presentation. 5-15% DSH patients suffer from some sorts of psychiatric disorders.
Motives/ reasons for DSH:
To die (really)
To escape from unbearable anguish.
To get relief (from some unbearable situation).
To change the behavior of others (which he/ she cannot do directly).
To escape from a situation.
To show desperation to others.
To get back at other people or make them feel guilty.
To get help (when some one is in danger and no one caring him).
Out come of DSH:
Repetition of suicidal attempts is based on group of patients and also on those who are on
psychiatric treatment. 15-25% repeats in the year after act. Risk factors: For further
attempt /suicide:

History of previous suicidal attempts.

Personality disorders (PD.)

History of alcohol and drug abuse

Unemployment in the patient

Lower social class

Criminal record in the past

History of violence by the patient

Age between 25-54 yr

Single, divorced / separated.
Result of Psychiatric intervention:
Who had been assessed by psychiatrist-- The rate of suicidal attempt repetition was 1/2
than those of the patients who were discharged with out psychiatric assessment
Provision of emergency contact card:
Some patients while being discharged are supplied with emergency contact card. This is
especially important for depressive patients who can consult their doctors as soon as
suicidal intend or impulse is there. * Dialectic behavior therapy should be done for chronic
repetitive /self harm / abnormal personality character group of patients.
Well organized Psychiatric care:
1) Enables recognition and treatment of major mental cases. 2) Provides appropriate care
for a range of personal and social difficulties.
Assessment after DSH:
a) Immediate risk of suicide in the patient.
b) Subsequent risk of further DSH in future.
c) Current medical/ social problem.
d) Encourage the patient to undertake a constructive view of his problem. The patient
is encouraged to consider the different ways he can avail to solve the problem on
himself.
Special inquiries:
We must be careful about the following facts while assessing the patients in the ward viz.
a. What are the pt's intentions when harmed himself?
b. Does he now intend to die?
c. What are the patient's current problems?
d. Is there a psychiatric problem?
e. What helpful resources are available to this patient?
What were the intentions when harmed herself?
a. Was the act planned/ carried impulsively?
b. Were precautions taken against being found?
C. Did the patient seek help?
d. Was the method thought to be dangerous?
e. Was there a 'final act' writing in suicidal note? Making a will?
f. Does he now intend to die?
g. Pleased to have recovered?
h. Wishes that he had died?
Clinician has to be tactful in asking genuine questions resolving the problem. As patients
some times misleads physicians about it.
What are the current problems?
a. The problems may be in terms of intimate relationship with spouse/ another person.
b. Intimate relationship with children/ other relatives.
c. Problems in employment, finance and housing.
d. There may be legal problem.
e. Social isolation, bereavement/other loss.
f. Drug and alcohol problem with psychiatric illness.
Is there a psychiatric disorder?
It should be properly assessed whether there is any
* Depressive illness
* Personality disorders
* Schizophrenia
Adjustment disorder
Substance and alcohol abuse
Impulse control disorder
* Dementia (rarely)
Management:
DSH should preferably be dealt by qualified psychiatrist; if not available the following
management guideline should be applied.
Encouragement of self help:

Is very important for those who wish not to be seen by psychiatrist.

Interview should be done in a room not overheard/ interrupted.

Assessment should be done after full recovery to give details of poisoning. Then
the information to be taken from the relatives, friends or family doctors who
attempted help to the patient first.
Is treatment required and will the patient agree to it?
5-10% DSH needs psychiatric unit admission after being managed in the general ward.
They need treatment for depression, alcoholism and Schizophrenia. Others need only
domestic stress support relatives, careers, social workers. Problem oriented counseling for
personal problems is a very smart way of dealing with the problems.
Factors suggesting high suicidal intent.
i. Act carried out in isolation.
ii. Act timed so that intervention is unlikely.
iii. Precautions taken to avoid discovery.
iv. Preparation made to anticipation of death( making will, insurance).
V. Preparation made for the act (saving tablets).
vi. Communication of intends to others beforehand.(To doctors, friends,
family members)
vii. Leaving a suicidal note.
viii Not alerting potential helpers after the act.(shouting/calling for help)
Special group of patients needing special care:
a) Mothers of young children
 Associated with child abuse.
 Attitude to children and their welfare must have to be assessed.
b) Children and adolescents:

Common after 12yr.
 More in girls except at younger age.
 Drug over dose -more common.
 Dangerous amongst boys.
 To communicate distress, escape from stress.
 History of broken homes,
 F/H of psychiatric disorder and child abuse.
 Precipitated by difficulties with parents, friends/school work.
 Mood disorder and personality disorder.
Management:

Require Admission in psychiatry unit to be identified and receive specific
treatment.

1/3 has clear mental problem and need further treatment on OPD basis.

Rest 2/3 got less clear strategy.

Once they left, they may disincline to take any treatment.So it is needed home visit
and social worker follow up.
Who are offered follow up and attend:
a. Main aim of treatment is to enable them to resolve the difficulties that lead the act.
b. To deal with future crisis without further DSH.
c. Start with list of problems complied with assessment.
d. Encouraged to consider what step they could take to resolve.
e. To formulate a practical plan for tackling them one at a time.
f. To persuade the patient to do as much as possible on themselves.
Patient with interpersonal problem:
To interview other person involved alone first, and then jointly.
Couple can then solve their problem.
In Bereavement:
Sympathetic listening first, then encourage to seek ways of gradual rebuilding of life
without the person.
Appropriate measure depends on loss type by death, break up of marriage or end of a
relation.
Patient refusing psychiatric assessment:

Refuses interview, seeks discharge.

They have a high rate of repetition

So try to get as much as information possible from other sources to exclude serious
suicidal intend
*On leaving hospital:
Liaison with local community based mental services.
Often detention under compulsory order is appropriate.
Involvement of family members in treatment.
Chapter-16
Travel Related Poisoning/Commuters poisoning
Lesson: 16
Subject: Travel related poisoning
Objectives:
 Tell about situation of induced
poisoning in Bangladesh.
 Describe the mode and pattern of
poisoning.
 Tell the management of travel
related poisoning.
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Introduction: Poisoning is an important health problem in Bangladesh causing around
3,00,000 episodes and around 2,000 death per year (Bangladesh Health Bulletin 2001).
There was a change in the trends of pattern of poisoning over the recent decades from
Endrine poisoning to Organophosphorus compound poisoning as an agent of attempted
suicide; from "Dhutura" poisoning to unidentified stupefying agent particularly during
journey.
The poisoning occuring during. movement using public transport is an emerging social and
public health concern in Bangladesh. This emergency health problem was not adequately
addressed in Bangladesh before. Few years back it was observed to be induced with
"Dhutura" and allied compounds, now different benzodiazepines are used with different
food items for this purpose
This is a very painful experience for the victim, for the trainee doctors, for the nurses, and
for the police concerned. The incidence of this type of induced poisoning in cities like
Dhaka, Chittagong, Rajshahi, Khulna is increasing during festival time like Eid ul fitr, Eid
ul azha, Durga Puja, etc.
Situation of induced poisoning in Bangladesh:

There is no clear cut data about travel related poisoning as no remarkable study has
been done in this issue.

On average, 1-2 patients/day with induced poisoning on journey used to get
admitted during festival time.

A study conducted by Mahbub et al in one adult Medicine unit in Dhaka Medical
college from Jan, 2004 to July, 2004 found that 172 patients were admitted due to
induced poisoning which was 9.26% of total admitted patients and 49.3% of total
poisoning patients.

From August, 2005 to July, 2006 total 319 patients (55.86% of total poisoning
patient) were admitted in one unit due to travel related unknown poisoning
(Hospital register books, DMCH).
Mode and pattern of induced poisoning:

The miscreants use tea, coffee, biscuit, 'dab water', cold drinks, fruit, fruit juice,
betel nut, 'jhal muri', etc in bus, train, launch, railway station, 'maxy' stand, bus
stand. Sometimes they offer medication of low cost for some disease like skin
disease, asthma, hemorrhoids.

Majority (70%) of people were made stuporus with dab water, soft drinks and tea.
Smaller percentage of victims is offered betel leaf with nut, cream biscuits, and
fruit juice. These agents are chosen as they are popular fast food, cheaper to buy
and easily available and widely accepted.
11

Majority of victim travels through bus. More incidence of induced poisoning
occurred when they are returning home from office. Probably at that time they are
hungry so that they took dab water, tea, biscuit, 'jhal muri' etc. Moreover at that
time they may have salaries with them and they are more relaxed.

Police with the help of bus staff initially rescued victims. The police then get them
admitted through emergency into Hospital. Hundred percent of victims do not
receive any prior hospital treatment - this indicates people with no money is still
dependent on the service of government Hospital.

There is exclusively male sex pre-ponderance in induced poisoning cases, 86%
compared to 14% which differs from result of nationwide survey of poisoning in
2002 in which male female ratio was 59.4% : 40.6% (Nationwide survey of pattern
of poisoning in Bangladesh- unpublished data).

Most of the victims had lost their valuables including money. This indicates the
purpose of this sort of poisoning. Sometimes the people are robbed of their
mobiles, wristwatches, wedding rings, credit-cards, official documents. This nature
depicts the purpose of miscreants and describes that the miscreants act in groups in
different places as small group taking it as a profession, making the people and
police fool and rob their valuable in regular basis. They may be linked with larger
chain of miscreants and this needs to be identified by the law-enforcing agencies of
government to disrupt the chain and to protect the people of being robbed off
during journey.

These patients are admitted throughout the year but interestingly more during
summer possibly people are usually thirsty due to excessive hot weather and easily
deceived with an offer of cold drink from other person (Hospital records).
Clinical Features and Investigation:

The interesting aspect of change of pattern of poisoning happened in the nature of
patients of unknown poisoning from Datura to sedative which can be differentiated
by skin condition, pupil size, relatively calm patient with uneventful recovery.

Majority of victims were unconscious within 30 minutes of time after ingestion of
offered substance and remaining were unconscious within 60 minutes because
hypnotics used were absorbed quickly from gut, acted rapidly on central nervous
system and made the person stuporous.

Patient are usually brought by police in a drowsy or stuporous conditions. Systemic
examination is usually normal with no focal neurological deficit.

Laboratory investigations including haemogram, Kidney function test, ECG
examination are unremarkable in most cases.
Management:
The patients are usually managed in a very busy admitting unit. Many patients are
managed in hospital floor. Few patients had accompanying relatives with them. Hospital
facilities, logistics and staff cannot cope with such number of admitted patients. Young
trainee doctors and nurses managed the patients with resource limitations. Usually this
type of victims does not require specific treatment other than maintenance of nutrition,
fluid replacement and nursing care. Fortunately most of the patients are discharged within
24 hours after admission uneventfully.

Almost all patients are given stomach wash as a part of management of general
poisoning, which did not reveal any significant gastric aspirate colour.
12

Usually almost all patients are recovered fully. Some of them absconded probably
due to social and medico-legal cause. Absence of mortality among suspected
induced poisoning is reassuring for us.
Conclusion:

The incidence is increasing and pattern is changing day by day as urbanization is
going on.

Community-based studies are needed to identify the problem on nationwide basis
and formulate a uniform guidelines about treatment,

Special measures should be taken for management of cases.

The facility of chemical identification of the induced poisoning should be made
available for more effective, specific treatment of the patients rather relying on
supportive treatment only.

Special measures should be taken by the hospital administration for urgent
management of these unaccompanied victims.

Steps should be taken by law-enforcing agencies to identify the offending agents
and culprit by vigilance.

Advice should be given to the public not to take food items on the travel
particularly from an unknown person.

Social awareness for safe travel needs to be created.
References:
(1) Bangladesh Health Bulletin, UMIS, Directorate General of Health Services.
(2001); vol7:121-122
(2) Fiaz M A and Hasan M. Situation of poisoning in Bangladesh. Country Report in
SAARC meeting on Poisoning Colombo, Sri Lanka. (1999);1:31-32
(3) Uddin M J. Shahed F H, Bhowmik S K et al. Transport related poisoning an untapped
public problem. The Healer (2002). 9 (2). 40-42.
(4) Mohammad Robed Amin, Sheikh Mohammad Hasan Mamun, Mohammad Ali,
Mohibur Rahman, Abdullah Al Hasan, M. Ridwanur Rahman & Mohammad Abul
Faiz: Poisoning While Traveling (Transport Poisoning): Is It A New Entity?: The Internet
Journal of Tropical Medicine. 2008; Volume 5, Number 1:4-6
(5) Mahbub Alam Majumder, Murshidur Rahman Khan, Sakina Anwar, Shamshul
Alam, M.A.Faiz et al. A clinical study on travel related poisoning. Abstract book of 5th
National Conference and Scientific Seminar of Bangladesh Society of Medicine;
December( 2004); 1:5-6
(6).Jain A and Bhatnagar MK. Changing trends of poisoning at railway stations. (2000).
JAPI ;48: 1036.
(7).Azhar et al. Poisoning pattern in medical outdoor- is it changing. TAJ (Raj). (1994);
2:7.
(8).Buckley NA, Dawson AH, Whyte IM, O'Connell DL: Relative toxicity of
benzodiazepines in overdose. BMJ 1995 Jan 28; 310(6974): 219-21.
Chapter 16
Prevention of poisoning
13
Duration: 01 hour
Objectives:
 Describe the concept and major steps of
poisoning prevention
 Tell the different aspect on how to make
home safe
 Describe the prevention mechanism of
pesticide poisoning

Tell the prevention measures about
snakebite, insects bite, poisonous plant
poisoning and food poisoning
Sl
no
01 Ice breaking and

05
Transparency/Flip
Introduction to the
minutes
and answer
chart
session
02 concept and major

10
Presentation,
Multimedia, Board,
steps of poisoning
minutes
discussion,
Marker,
prevention
Question and answer
Transparency/ Flip
chart
03 Different aspect on
15
Presentation,
Multimedia, Board,
how to make home safe

minutes
discussion,
Marker,

Transparency/Flip
Case presentation
chart
04 Prevention measures
20
Presentation,
Multimedia, Board,
about snakebite, insects

minutes
discussion,
Marker,
bite, poisonous plant

Transparency/ Flip
poisoning and food

Case study
chart
poisoning
05 Summarization 05
Discussion,
Board, Marker,
minutes
Question and answer
Transparency / Flip
chart

05

minutes
chart
participants
14
15
Introduction:
Prevention of Poisoning
It is better, safer and cheaper to prevent poisoning than to cure it. Most poisonings can be
prevented. Everyone - children, parents, farmers, schoolteachers, factory workers and
health care workers - can do things to make their homes, their workplaces, and the
community safer.
There are three steps we should take:
(a)
First of all, find out about the poisonings that have happened in your community in
the last few years. Find out how they happened, where they happened and what the
poisons were. Think about why the poisonings happened.
(b)
Think about how poisonings that have happened in your community could have
been prevented.
(c)
Discuss with people how poisonings can be prevented. Share what you know with
others and help them understand why poisonings happen and what can be done to
stop them happening again.

Talk with families and mother-and-child health groups about preventing
poisoning at home. Talk about how to teach children, even at an early age, not
to touch, eat or play with medicines or household chemicals.

Talk to schoolteachers about how to teach children about the dangers of
poisoning in their homes and the dangers from poisonous snakes, plants and
animals.

Talk to community leaders or committees about the accidents that have
happened.
It is important to handle all chemicals safely, not just the ones you know are poisons.
Many chemicals that you might not think are poisonous could make someone ill or cause
burns. It is very important to protect children, because they cannot protect themselves and
they do not understand that some things can be poisonous.
Keep chemicals safely

Do keep medicines, cleaners and pesticides where children cannot see or reach
them

Do not keep chemicals you no longer need.

Do not put chemicals in containers that once contained food or drink; people may
eat or drink the chemicals by mistake.
Use chemicals safely

Do use medicines, cleaners, pesticides and other chemicals in the right way, and
use the right amount (not more or less). Read the label and follow carefully the
instructions for use. A person who cannot read it should find someone who can. It
may be dangerous to use chemicals from unlabelled containers. Ask the supplier
for another container with a label.
Get rid of left-over chemicals and empty containers safely

Do find out whether it is better to bury or burn the chemicals you want to get rid of.

Do not use empty bottles, cans or other containers that have been used for storing
chemicals to store or cook food or drink.

Do not give them to children to play with.
16
 Do not throw left-over chemicals or empty containers near a river, pond or spring.
How to make homes safe
How to keep chemicals safely
Do keep all household chemicals where children cannot see them or reach them. Keep
medicines, insecticides, weed killers and rat poison in a locked cupboard or locked
suitcase or in a high cupboard.
Do keep household products, pesticides and medicines in their own containers.
Do keep caps and tops on bottles and keep them properly closed.
A child who finds an open container may swallow the contents before anyone can stop him
or her. A child may try to open a closed container, but this may take time and a young
child will often find it difficult. An adult may see what is happening and stop the child
before he or she can open the container.

Do not keep household cleaners on the floor, under the kitchen sink, or in low
cupboards that a child can easily open

Do not keep medicines, pesticides or household products next to food or drink.

Do not keep chemicals or empty containers you no longer need.

Household chemicals, such as cleaners or pesticides

Do read the label. Make sure you know how to use the product and how much to
use, and look for advice about how to use the product safely.

Do hold on to a product while you are working with it. If you put it down, leave it
where you can see it all the time. A child can quickly grab an open bottle and
swallow the liquid, or spill it onto the skin or into the eyes.

Do wipe up any of the chemical that gets spilt, and make sure the outside of the
bottle or container is clean and dry.

Do put chemicals away as soon as you have finished using them.

While they are out of their usual storage place, children may get hold of them.

Do not spray household pesticides over food or children's toys.

Do not mix different cleaners or other products together.

If the product has to be added to water before it is used, do not mix it in a container
that is used for food and drink.
How to prevent poisoning with pesticides
Pesticides are very widely used and in some countries many people get sick or die because
of poisoning with pesticides. Poisoning can be prevented if pesticides are used safely and
proper precautions are taken.
Store pesticides safely

Do keep pesticides in their original containers.

Do keep pesticides in a safe and secure store.

Do make a list of all products in the store and update it regularly.

Do keep pesticides, particularly rodenticide baits and pesticide treated seeds, away
from foodstuffs so they are not mistaken for food.
17

Do not keep agricultural pesticides in living areas. Keep them in a separate shelter.

Do not keep pesticides in drink bottles or other containers normally used for food
or drink.
Use pesticides safely
Everyone who applies pesticide should first have training in the method of application, the
operation, cleaning and maintenance of the equipment and the safety precautions to be
taken.

Do read the label and any other product information you have been given, before
you use the product. If you do not understand the information, ask someone
who knows, such as your employer or the person who supplied the product.
Never use a product until you have read and understood the label of clothing or
equipment it is because the product could harm or even kill you if you do not
have that protection.
Make sure all protective clothing and equipment are properly checked,
maintained and stored.

Do mix only the amount of chemical that can be used in one day. Then you will
not need to get rid of left-over pesticide or leave it overnight.

Do have plenty of soap and water available for washing.

Do wash gloves before you take them off.

Do wash your hands thoroughly with soap and water after handling or using
pesticides. Wash your hands with soap and water before you eat, drink, chew
tobacco, smoke, rub your eyes or touch your mouth.

Do make sure that you are never alone when you are mixing or using very
poisonous pesticides.
Stop work immediately if you are using a chemical and you get a rash or feel
sick, if your eyesight troubles you, or you begin to sweat more than usual or feel
unusually thirsty, or even if you have a headache or cold or flu symptoms. Tell
your employer and go to a doctor at once. Show the product label, information
leaflet or data sheet to the doctor.

Do find out when it is safe to harvest and eat food that has been sprayed with
pesticide.

Do bury or burn food that has been contaminated by pesticide.

Do not use dirty or damaged protective equipment, or dirty or torn protective
clothes, or leaking gloves or boots. They may be more dangerous than using
nothing.

Do not use bare hands to scoop powder out of packs, or dip bare arms or hands
into liquids to stir mixtures. Use measures and mixing vessels for making up
solutions. Do not use these for anything except pesticides.

Do not measure out or mix pesticides in or near houses, or where animals are
kept.

Do not blow through or suck spray nozzles to clear blockages.

Clean the nozzle with water or a grass stem.

Do not spray pesticide when a strong wind is blowing because it may drift over
you, or nearby animals or houses.

Do not leave pesticides unattended while they are out of the store.

Do not let anyone go into fields when pesticides are being sprayed.
18

Do not let children drink or play near spray equipment or near places where
pesticides are mixed, or near a field that is being sprayed.

Do not let children use pesticides.
Getting help and taking people to hospital
The easiest way to get help when there is an accident at work is to shout to a fellow-
worker or, for those working at home, a member of the family or a neighbor.
Employers should know what to do and who to contact if there is an accident or emergency
with dangerous chemicals.
How to avoid snake bites : Describe In chapter 13
How to prevent insect, spider and scorpion stings and bites

Do find out about the poisonous insects, caterpillars, spiders, and scorpions in your
area. Learn what they look like and where they live.

To protect you from bee stings when working among flowers or fruits, do wear
long trousers, long-sleeved shirts and gloves, and cover your head and face as
much as possible. Avoid wearing things that attract bees, such as bright flowery
Clothing, bright shiny jeweler buttons or buckles, or using scented perfume, soap
or shampoo.

Do not walk outdoors in bare feet or open shoes.

Do not touch insects, caterpillars, spiders, scorpions

Do not put your hands in leaf litter, rotten tree trunks or holes where insects,
caterpillars, spiders, scorpions or centipedes might live.
How to avoid eating poisonous plants, mushrooms and fish

Do find out which plants and mushrooms in your community are poisonous and
what they look like. Make sure you can recognize them - some edible plants,
mushrooms and fish are very hard to distinguish from poisonous ones.

Do learn how to prepare foods correctly. Some plants (like cassava) are poisonous
if not properly prepared or cooked, and some plants and fish have poisonous parts
that must not be eaten.

If you are preparing tropical fish, do separate the flesh from the head, skin and gut
as soon as possible, because these may contain large amounts of poison.

Do not buy mushrooms from people who are selling them by the roadside.

Do not eat fish that is not fresh. Some fish are good to eat when they are fresh, but
become poisonous when they have been dead for some time.
How to avoid infection from food contaminated with germs

Do keep kitchens clean. Keep tables and other surfaces on which food is prepared
clean, and keep kitchen utensils clean.

Do protect food by keeping it covered or in boxes or cupboards with wire screens.

Do wash your hands well with clean soap and water before touching or preparing
food. Cuts or sores on fingers should be covered with a clean dressing.
19

Do boil plates and eating utensils used by sick people before anyone else uses
them.

Do not keep food for a long time in a warm place. Do not keep left-over cooked
food if you cannot keep it cool or keep it in a Refrigerator.

Do not let flies, other insects, worms, rats or other animals touch or crawl on food.
They carry germs and spread disease.

Do not let dust get on food or let people touch food.

Do not leave food scraps or dirty dishes lying around, as these attract flies and let
germs breed.

Do not leave clean utensils lying on the ground.

Do not eat raw or undercooked meat. Cook it right through.

Do not eat food that is old or smells bad.

Do not eat food from cans that are swollen or that squirt out when opened. Be
especially careful with canned fish.
Annexure 1: First Aid for poisoning patient
First aid is the help a person gives straight away in a medical emergency.
This chapter can help you learn first aid, but you also need someone to teach you first aid,
and check that you are doing it correctly. It is important to have someone show you the
right way to do mouth-to-mouth respiration and heart massage. You should practice on a
special training manikin (a life-size model). Never practise heart massage on another
person, only on a manikin. It is dangerous to use heart massage if you have not had proper
training.
People who are poisoned may:
- be unconscious,
- stop breathing,
- have no heartbeat,
- have fits (convulsions).
They need immediate first aid to help them to breathe and to start the heart beating.
When people get chemical in the eyes or on the skin, it may cause burns. These people
need immediate first aid to wash the chemicals out of the eyes and off the skin. The
chemical may also get into the body and cause poisoning. Immediate first aid may stop
serious poisoning and may save life. If breathing and the heart stop, the person will die
within a few minutes unless you give first aid at once.
First aid for poisoning
Here is an action list. Each step is explained in more detail below the list. Start with the
first step and follow each step in the order given. Act as quickly as you can, but stay calm.

Check if the patient is conscious.

Open the airway and make sure the tongue is not blocking the throat.

Check if the patient is breathing.
20

Clean out the mouth and clear the throat.

Give mouth-to-mouth respiration.

Check if the heart is beating.

If the heart is beating, but the patient is still not breathing, carry on with
mouth-to-mouth respiration.

If the heart is not beating, give heart massage.

If the patient is breathing but is unconscious, turn him or her onto one side, into the
recovery position.

Give first aid for fits if necessary.

Wash any chemical out of the eyes.

Remove contaminated clothing and wash any chemical off the skin and hair.

Give first aid for poisonous bites and stings.
Check if the patient is conscious:
Try to make the patient wake up. Shout "Are you all right?" and gently shake the
shoulders, but take care not to make any injuries worse (Fig. 1). Pinch the skin on the neck
and watch the face. A patient who is just sleeping will wake up, but an unconscious
patient will not.
Open the airway:
In an unconscious patient the tongue may block the throat and the airway. Make sure the
airway is open and air can get down the throat (Fig. 2): Place the patient on his or her back.

Tilt the head back and lift the chin up with the finger and thumb of one hand on the
bony part of the chin, while pressing the forehead back with the other hand (Fig.
2). This will open the airway and stop the tongue blocking the throat.
21
Check whether the patient is breathing:
After opening the airway, quickly check whether the patient is breathing (Fig. 3):

Look for the belly or the chest moving up and down.

Feel the chest moving up and down.

Feel the patient's breathe on your cheek.

Listen for breath sounds. Put your ear close to the patient's mouth.
Use all four checks. Remember that the chest may move up and down even when the
throat is completely blocked and air cannot get to the lungs.
A person may stop breathing because:

Something is stuck in the throat.

The throat is blocked by the tongue, or by blood, spit, vomit, food, or false teeth.
(If you have tilted the head back, the tongue will not block the throat.)

The throat is blocked because the patient has swallowed poison which has burnt the
throat and made it swell.

The patient has been poisoned.

The patient has been hit on the head or chest.
22

The patient has had a heart attack.

The patient has nearly drowned.
Clean out the mouth and clear the throat:
If the patient is not breathing after
you have tilted the head back,
something may be blocking the
throat.
Turn the head to one side. With
one or two fingers (and preferably
wearing gloves) scoop deeply
round the mouth and throat to clear
any blockage such as vomit (see
Fig. 4). Take out the patient's false
teeth.
If the patient starts breathing turn him or her onto one side, into the recovery position.
Check breathing and pulse frequently.
Whatever the cause, if the patient does not start breathing you must act immediately to
help the patient to breathe.
Give mouth-to-mouth respiration:
You can help the patient to breathe by blowing air from your lungs into his or her lungs
through the patient's mouth (mouth to mouth) or nose (mouth to nose). This is called
mouth-to-mouth (or mouth-to-nose) respiration.
* Do not give mouth-to-mouth respiration if the patient is still breathing.
If there is poison on the patient's lips, or if corrosive chemicals have burnt the lips and
chin, wipe the chemical off, cover the mouth with a cloth to protect yourself from getting
poison on your lips or hands, and give mouth-to-nose respiration. Breathe into the patient's
nose (see Fig. 5)
23
How to give mouth-to-mouth respiration or mouth-to-nose respiration to an adult:
1. With the patient lying flat
on his or her back, clear
any blockage from the
mouth. Kneel beside the
patient's head.
2. Tilt the head back.
3. Pinch the nose with one
hand. With the other hand
pull the mouth open
(Fig. 6).
4. Do not press on the neck.
For mouth-to-nose
respiration, close the
patient's mouth with your thumb.
5. Breathe in deeply Cover the patient's mouth completely with your own mouth and
breathe out steadily and smoothly so that all your breath goes into the patient's mouth.
Breathe out strongly to fill the chest (see Fig. 7). Look for the patient's chest rising. For
mouth-to-nose respiration put your mouth around the patient's nose.
6. Lift your mouth away so that the patient can breathe out and you can take another
breath of air. Turn your head, look for the chest falling, feel the breathed-out air on
your cheek, and listen for the sound of the patient breathing out (see Fig. 7). For
mouth-to-nose respiration you may have to open the patient's mouth to let air out.
7. Take another breath of air. Once the chest has fallen, blow into the patient's mouth (or
nose) again. Watch the patient breathe out again. Then check that the heart is beating.
If the chest does not rise with each breath, and you cannot feel or hear the patient
breathing out, then either the airway is blocked or some of your breath is not going into
the patient's chest. Check that the head is held well back and clear the airway again.
Make sure there is no air escaping when you breathe into the patient's mouth (or nose).
How to give mouth-to-mouth respiration to a child or a baby:
24
Open the airway in a child or
baby in the same way as for an
adult, but do not tilt the head too
far back or the soft airway may
kink.
If you can see something
blocking the throat carefully
remove it, but do not sweep your
finger inside a baby's mouth if
you cannot see anything there. If
the throat is swollen because of
an infection, you might make the
swelling worse.
Do not pinch the nose. Put your lips over both the nose and the mouth (Fig. 8). Breathe
gently, just enough to move the chest. For a very small baby only small puffs are needed.
Do not blow hard or you may harm the baby's chest. Blow into the chest every 3 seconds.
Check if the heart is beating:
Feel for the pulse in the neck. Place two fingers on the voice box (Adam's apple) and slide
your fingers into the groove under the jaw (Fig. 9). Keep your fingers there for at least five
seconds to feel if there is a pulse.
If you cannot feel a pulse, the patient is in cardiac arrest. The patient will be unconscious
and will probably have dilated pupils. If the patient has white skin it will probably have a
blue-grey colour. If the patient has black or brown skin look for a blue colour to the nails,
lips and the inside of the lower eyelids. If the heart stops, breathing will also stop and the
patient will need both cardiac massage and mouth-to-mouth respiration.
If the heart is beating, but the patient is still not breathing, carry on with mouth-to-
mouth respiration:
Take a deep breath and blow once every 5 seconds, until the patient starts to breathe
without help. You may have to do this for more than one hour.
25
If the patient has breathed in an irritant gas, the mouth and throat may be full of froth. You
cannot remove this froth by wiping, so do not waste time trying to remove it. As this froth
is air bubbles, all you have to do to move air in and out of the lungs is to blow the froth
into the lungs. So blow as usual.
When the patient starts to breathe, turn him or her onto one side into the recovery position.
The patient may vomit when breathing starts again but the vomit will not block the throat
if the patient is lying on one side. Let the vomit come out and clear it out of the mouth
with your finger.
Watch carefully in case the patient stops breathing again. If breathing stops turn the patient
onto his or her back and start mouth-to-mouth respiration again.
If the heart is not beating give heart massage
If you cannot feel a pulse in the neck, you should try to start the heart beating again by
giving heart massage.
Heart massage (or chest compression) means pressing down on the heart to push blood out
of it and round the body. This may start the heart beating again. It will only be effective if
the patient is lying on a hard surface.
If there is no heartbeat, the patient will have stopped breathing. Always start mouth-to-
mouth respiration before heart massage.
Do not give heart massage if the heart is beating, even faintly. Stop as soon as you feel a
pulse in the neck, but carry on with mouth-to-mouth respiration if the patient is still not
breathing.
How to give cardiac massage to an adult:
1. Check that there is no heartbeat.
2. Lay the patient on his or her back on a firm surface. Kneel beside the patient's
chest.
3. Find the right place to put your hands. Find the lower edge of the ribs. Follow the
edge of the ribs to where they meet the sternum. Place your middle finger on the
base of the sternum, and the index finger next to it (Fig. 10), then place the heel of
your other hand next to these two fingers, on the breastbone in the midline of the
chest.
4. Now cover this hand with the heel of your other hand, lock your fingers together,
keeping them off the chest (Fig. 10). Put your shoulders above the patient's chest
and keep your arms straight.
26
5. Press down on the lower half of the sternum 4-5 centimeters, keeping your, arms
straight. Then stop pushing. While counting "one and two and three and press 15
times, in time with the numbers (80 presses a minute). Presses should be regular
and smooth, not jerky and jabbing.
6. Remember that both mouth-to-mouth respiration and heart massage are needed.
After 15 presses tilt the head back again so that air can get down the throat, put
your mouth round the patient's mouth and give two breaths.
7. Continue with 15 presses followed by two full breaths. After one minute check the
heartbeat, then after 3 minutes or every 12 cycles check the heartbeat again. As
soon as the heartbeat returns stop heart massage immediately. You may see the
patient's colour become more normal and the pupils return to normal size.
8. Continue mouth-to-mouth respiration at 12 breaths a minute, until the patient
breathes without help. It may be some time before breathing starts again, even after
the heart has started beating. When breathing starts again put the patient onto his or
her side in the recovery position. If another person is with you, get him or her to do
the breathing while you do the heart massage (Fig. 11).
The other person should kneel by the patient's head while you kneel by the middle of the
chest. The other person should give two breaths and check the heartbeat. If there is no
heartbeat you should give five presses on the chest. Continue with the other person giving
one breath and you giving five presses on the chest. Check the heartbeat after one minute
then after every three minutes or 12 cycles.
27
How to give heart massage to a child or a baby:
The best place to feel the pulse in a small child or a baby is on the inside of the upper arm.
With your thumb on the outside of the arm press your first and middle fingers into the
groove below the muscle. When giving heart massage to a child or baby, press with less
force but slightly faster than
you would for an adult.
For a child use one hand only
and press lightly on the chest
(Fig. 12). Press down 2.5-3.5
cm. For a small child or a baby
press on the chest with just two
fingers. Press down 1.5-2.5 cm.
Keep your hand or fingers
below the level of the nipples.
Press down at a rate of 100 presses a minute giving 15 compressions followed by two
breaths.
If the patient is breathing, but is unconscious, turn him or her onto one side, into the
recovery position:
An unconscious patient should be turned to lie on one side to stop the tongue blocking the
throat and to allow fluid to come out of the mouth. This is called the recovery position.
Before you turn the patient over:

If breathing is noisy, sweep your finger round the mouth to remove anything
blocking the airway, and take out the patient's false teeth if they are loose.

Empty the patient's pockets of anything that would be uncomfortable to lie on.

Take off the patient's spectacles in case they injure the eyes.

Look for injury to the head or neck, and feel with your fingers to see whether the
back of the neck or the backbone is bent or swollen.

Get help if the patient has an injury to the head or neck. Three people should roll
the patient keeping the head, neck and body in a straight line. Do not let the patient
sit up when he or she wakes up.
28
The patient should be turned onto one side with:

the head, neck and body in a straight line, - the head placed so that the tongue will
not block the throat, and vomit or saliva can come out of the mouth
(Fig-13)

the arms and legs placed so that the patient stays in the same position.
One way of turning a patient:

Lie person on the side or front downwards, with head turned to one side.

If the person is to be transported, use this polture in order to prevent vomitus from
entering the lungs.

Never give anything by mouth to an unconscious patient.
(a)
Kneel beside the patient, turn the patient's face towards you, and tilt it back,
with the jaw jutting forward so the airway stays, opelh.- Place the arm nearest
you above the head. Place the patient's other arm across the chest. Raise the
patient's far leg under the knee, to bend it (Fig. 14).
(b)
Protect the patient's face with one hand. With your other hand, grasp the
patient's clothes at the hip and pull the patient towards you until he or she is
resting on one side, against your knees (Fig. 13, 14). The patient's head should
be resting on the lower arm. Check that the airway is still open.
(c)
t's upper arm and place the hand under the face (Fig. 14). This will help to keep
the head tilted back and the airway open. Now position the upper leg so that the
bent knee rests on the ground and supports the patient's body. If the patient is
too heavy for you, get help. Someone else can support the patient's head while
you do the turning, or can push the patient towards you as you pull.
Give first aid for fits (convulsions) if necessary:
(a)
If the patient has a fit, make him or her lie down in a safe place. Make sure there is
no hard or sharp object nearby and protect the patient from injury.
(b)
Turn the patient to lie on one side so that the tongue comes to the front of the
mouth and froth can come out of the mouth easily
(c)
Put a folded cloth under the patient's head, or hold the head so that it does not bang
on hard things.
29
(d)
Do not try to stop the shaking movements.
(e)
Loosen any tight clothing.
(f)
Do not put anything in the patient's mouth or try to open it.
(g)
After the fit, let the patient rest in the recovery position.
Wash any chemical out of the eyes:
Wash chemicals out of the eyes at once, with plenty of cool, clean water, before you wash
the skin. Even a delay of a few seconds can make the injury worse.
1.
Immediately gently brush or wipe any liquid or powdered chemical off the face. Let
the patient sit or lie down with the head tilted back and turned towards the worst
affected side. Gently open the eyelids of the affected eye or eyes and run cold water
over from a tap or pour water from a jug. Make sure the water drains away from the
face and does not go into the unaffected eye. Wash out the eye or eyes in this way
for 15-20 minutes, timed with a watch if possible.
The patient may be in great pain and may want to keep his or her eyes closed, but
you must wash the chemical out of the eyes in order to prevent permanent damage.
Gently pull the eyelids wide open, and keep them apart (Fig. 15).
2.
While you are rinsing the eyes check that the inside of the eyelids has been well
washed. Check that there are no solid pieces of chemical in the folds of skin round
the eyes, or on the eyelashes or eyebrows. If you are not sure whether all the
chemical has been removed, wash out the eyes for 10 more minutes.
3.
Do not let the patient rub the eyes.
4.
The patient's eyes should be examined by a doctor even if there is no pain, because
damage may be delayed
5.
If light hurts the patient's eyes, cover them with a sterile eye pad, a dry gauze pad,
or a pad of clean cloth. Bandage the pad in place securely, but not too tightly. This
will protect the eyes and help them to heal.
6.
If the patient is in pain, give aspirin or paracetamol every four hours.
Medical treatment of chemical contamination of the eye:
30

If the pain is severe the patient may need an intramuscular injection of morphine.

Look for burns. Put drops of fluorescein in the eye. Burns will stain yellow.

Prevent infection. If there are yellow stains with fluorescein, put chloramphenicol 1
% eye ointment in the eye. Put ointment into the eye every two hours. Continue
until the eye is no longer red and the sclera is white, and then for another 24 hours.
Remove contaminated clothing and wash any chemical off the skin and hair:
1 . Take the patient immediately to the nearest shower or source of clean water. If there is
no water nearby dab or gently wipe the skin and hair with cloths or paper. Do not rub
or scrub the skin.
2. Immediately wash the
affected part of the body
under cold or lukewarm
running water, using soap if
you have some. If there is no
running water use buckets of
water. Do it quickly and use
a lot of water (Fig. 16). Wear
gloves and an apron if
needed, to protect yourself
from splashes of chemical.
Some chemicals give off
vapour: be careful not to
breathe it in.
3. At the same time quickly remove any of the patient's clothes contaminated with
chemical or vomit, as well as shoes and wrist watch if necessary. Speed is important -
cut the clothes off if the chemicals are very poisonous or corrosive.
4. If large areas of the body are contaminated with chemical, wash the patient under a
shower or a hose. Remember to clean the hair and under the fingernails, in the groin
and behind the ears, if necessary.
5. Continue to pour water over the patient for 10 minutes or longer if you can still see
chemicals on the skin. If the skin feels sticky or soapy, wash it until the feeling
disappears. This may take an hour or more.
6. Make sure the water drains away freely and safely as it will have chemical in it.
7. Dry the skin gently with a clean, soft towel. If clothing stays stuck to the skin even
after water has been poured over it, do not remove it.
8. Remember that many chemicals can pass through the skin very quickly. Look for signs
of poisoning.
9. Put contaminated clothes in a separate sealed container and do not use them again until
they have been washed. Throw away shoes contaminated with chemical. If you have
used cloths or paper to wipe the skin, put these in a container and burn them.
31
Annexure 2: Glasgow Coma Scale (GCS) & Blantyre coma scale
The Glasgow coma scale
Score
Eyes open: spontaneously 4
to speech 3
to pain 2
never 1
Best verbal response: oriented 5
confused 4
inappropriate words 3
incomprehensible sounds 2
none 1
Best motor response: obeys commands 6
localizes pain 5
flexion to pain:
withdrawal 4
abnormal 3
extension to pain 2
none 1
Total 3-15
In general a score of 8 or less is correlated with a poor prognosis. A score of 3-4 has an
85% chance of mortality.
The modified Glasgow coma scale (The Blantyre coma scale)
Score
Eye movements: directed (e.g. follows mother's face) 1
not directed 0
Verbal response: appropriate cry 2
moan or inappropriate cry 1
none 0
Best motor response: localizes painful stimulus1 2
2
withdraws limb from pain 1
nonspecific or absent response 0
Total 0-5
32
Annexure 3: Dosage of poisoning antidotes:
Poison Antidote
Aluminium Desferrioxamine
Arsenic Dimercaprol (BAL), DMSA
Benzodiazepines Flumazenil
ß-adrenoceptor blocking drugs Atropine, glucagon
Copper Dimercaprol, D-penicillamine, DMPS
Cyanide
Oxygen,dicobaltedetate,hydroxocobalamin, Sodium
thiosulphate
Digoxin and digitoxin

Digoxin-specific antibody fragments
Ethylene glycol Fomepizole, Ethanol
Iron salts Desferrioxamine
Lead (inorganic) Sodium calcium edetate, DMSA
Methaemoglobinaemia Methylthioninium chloride (Methylene blue)
Methanol Fomepizole, Ethanol
Mercury (inorganic) DMPS
Opioids Naloxone
Organophosphorus compounds Atropine, Pralidoxime or obidoxime
Paracetamol N-acetylcysteine, Methionine
Thallium Prussian (Berlin) blue
Warfarin and other anticoagulants Vitamin K1
a) Desferroxamine:( Desferroxamine, Desferol)
Indication: A) Iron poisoning. S. Iron >450-500pgm/dl or with significant s/s of
iron poisoning.
B) Aluminium poisoning
Dosage: Inj Desferroxamine IV infusion 15mg/kg/hr.
Inj Desferroxamine IM 40-90mg/kg every 8 hours. ( max 1 gm in
children, 2gm in adults)
Maximum cumulative daily dose-6gm.
End points of treatment- Normal urine color or serum Iron level
<350pgm/dl and resolution of clinical signs.
b) DMSA:( Dimercaptosuuccinic acid, Succimer)- Analogue of BAL
Indication: Lead, Zinc, mercury and arsenic poisoning.
Dosage: Per oral -1Omg/kg (or 350mg/M 2) 8 hourly, 5 days.
Then 12 hourly for 2 weeks
Formulation: Cheemet 100mg capsule. USA formulation.
c) Dimarcaprol:( British Anti-Lewisite)( BAL)
Indication: Arsenic, mercury, gold, zinc, copper and lead poisoning
33
Dosage: 3 mg/kg deep intramuscular(IM) every 4-6 hours for 2 days then 12
hourly for 7-10 days or until recovery In severe case 5mg/kg may be used.
In Lead poisoning: 4-5 mg /kg deep IM every 4 hours for 3-5 days for
symptomatic acute encephalopathy or serum level > 100pgm/dI
d) Dimercaptopropane-1-sulfonate (DMPS)- Analogue of BAL
Indication: Arsenic, mercury, gold, zinc, copper and lead poisoning
Dosage: 5mg/kg 6-8 hourly for 3-5 days
Formulation: IV and oral
e) D-Penicillamine:
Indication: Lead, mercury, copper and gold.
Dosage: 20-30mg/kg/d in 3-4 divided dosages. Starting dose in adult 250mg 4
times daily. maximum-4gm. It should be given in empty stomach 1 or
2 hours before a meal
Formulation: Cap. Artamine 250 mg.
f) Glucagon:
Indication: Beta blocker intoxication induced hypotension, bradicardia or
conduction defect.
Dosage: 5-1 Omg IV followed by 1-5mg/hour infusion
Formulation: Glucagon for injection, 1 unit and 10 units.
g) Digoxin-specific antibodies
Indication: Digoxin poisoning.
Dosage:
If ingested dosages is known
Tablet ingested
Tablet ingested
Approximate dose
Recommended
(0.125mg size)
(0.25mg size)
absorbed (mg)
dose (no. of vials)
5 2.5 0.5 1
10 5 1 2
20 10 2 4
50 25 5 10
100 50 10 20
NB. Should be given over 30 minutes IN. Bolus in life threatening dysarrythmia
If ingested dose is unknown
10 and 5 vials for acute or chronic poisoning respectively in adults
Formulation: Digibind 38mg per vial.
h) Methylene Blue:
34
Indication: Methhaemoglobinaemia.
Dosages: 1-2 mg/kg IV slowly over 5 minutes, Repeat dose in 30-60 min. If no response
after 2 dosages stop further dosing. NB. It turns urine into blue or green.
Formulation: 1% methylene blue injection (1 0mg/ml).
i) Vitamin K1
Indication: Coumarin induced excessive anticoagulation (High Prothrombin time)
Dosages: Oral: 10-25 mg/day in adult and 5-10mg/day in children.
Subcutaneous: Adult-5-10mg. Children-1 -5mg. Repeat in 6-8 hours
NB: Check PT after 24 hours
Intravenous route: Rarely use and only when haemorrage is present.
Adult- 20 mg slow IV; Children-0.6mg/kg under 12)
Repeat 6-8 hours; Caution-Anaphylactoid reaction
j)Atropine: Describe in Chapter 3
k) Pralidoxime /Obidoxime : Described in Chapter 3
l) Flumazenil : Describe in Chapter 4
m) N acetyl cysteine: Describe in Chapter 12
n) Methionine: Describe in Chapter 12
o) Ethanol: Describe in Chapter 8
p) Fomepizole( 4 methyl pyrazole):Describe in Chapter 8
q) Naloxone-
Indication: Opiate poisoning
Dosage- 0.8 mg to 2 mg iV. Repeat at intervals of 3 minutes to maximum dose
of 10 mg; NB- short half life.
IV infusion at a rate o 0.4-0.8 mg/hour (Adult); 0.03mg/kg (children)
r) Prussian Blue :
Indication: Thallium poisoning
Dosage: 5-10 g . Repeat 1 g three times a day orally or NG tube until
urinary thalium is less than 0.5 mg/24 hours
Formulation : Oral
s) Sodium Calcium Edetate:
Indication: Lead Poisoning
Dosage: 15-40 mg/kg in 500 ml of 0.9% sodium chloride or 5% dextrose
35
infusion over 1 to 2 hour twice a day for 5 days
Formulation: IV
o) Sodium Thiosulphate:
Indication: Cyanide poisoning
Dosage- Adult-50 ml of 25% sodium thiosulphate (12.5 g) IV over 10 min
Children< 25 kg- 1.65 ml/kg of 25% solution
p) Dicobalt edetate :(Kelocyanor)
Dosage –Adult-20 ml solution (300mg) IV over 1 minute followed by 50 ml of
50% dextrose IV
q) Hydroxycobalamin: (Vitamin B12)
Dosage – Adult: 10 ml of 40% hydroxycobalamin solution (4g) IV over 20 min
Children: 50 mg/kg
Available Registered Public Health Pesticides in Bangladesh:
Sl
Common Name of Products Trade Name of Products
No
1 d-allethrin ACI King Mosquito Coil
2 Sulphur Sulphotox 80 WP, Ronovit 80 WG, Thiovit
80 WG, Gayvet 80 DF, Multiplex 80 WP
3 Propargite Sumite 57 EC
4 Fenpropathrin Denitol 10 EC
5 Tertradifon Tedion V 18 EC
6 Hexathiazox Hexarite 5 EC
7 Carbendazim Bavistin DF, Amicozim 50 WP, Forastin 50
WP, Goldazim 500 SC, Baizim 50 WP
8 Carboxin+Thiram Vitavax 200B
9 Difenoconazole Score 250 EC
10 Edifenphos Edifen 50 EC, Hinosan EC 50
11 Copper oxychloride Cupravit 50 WP, Sunvit 50 WP
14 Iprodione Rovral 50 WP, Rovanon 50 WP,
15 Mancozeb Nemispore 80 WP, Razland 80 WP,
Dithane M 45
16 Propiconazole Proud 25 EC, Potent 250 EC, Conazole 25
EC
36
17 Benalaxy+Mancozeb Galben M
18 Metalaxy M+ Mancozeb Ridomil Gold MZ 68 WP, NUben 72 WP
19 Hexaconazole Anvil 5 SC, Conza 5 EC
20 Tebuconazole Folicur EW 250
21 Phenamidone+Mancozeb Secure 600 WG
22 Metenoxam+Chlorathalonil Folio Gold 440 SC
23 Accphate Tidphate 75 SP, Fortunate 75 SP
24 Azadirachtin Nimbicidine
25 Acetamipirid Platinum 20 SP
26 Abamectin Vertimec 1.8 EC, Acamite 1.8 EC
27 Osfencard (BPMC) Baycarb EC 500, Paprika 50 EC
28 Carbaryl Sevin 85 SP
29 Carbofuran Carbofuran 3G, Furacarb 3G, Razfuran 5G,
Brifur 5G
30 Cartap Car 4G, Car 50 SP, Baitap 50 SP, Nutap
4G, Bravo 50 SP, Classic 20 EC, Pychlorex
20 EC, Pyriban 15G, Baifos 20 EC, Gola
48 EC
31 Cypermethin Cythrine 10 EC, Cyperin 10 EC, Caught 10
EC
32 Profenofos Q+Cypermethrin Shobicron 425 EC
33 Lambda Cyhalothrin Fighter 2.5 EC, Dects 2.5 EC, , Acithrin 2.5
EC
34 Diazinon Razdan 10G, Diazonyl T 60 EC
35 Dimethoate Rogor 40 L, Dimezyl 40 EC
36 Endosulfan Thiodan 35 EC, Endosul 35 EC
37 Emramectin Benzoate Proclaim 5 SG
38 Fenthion Lebaycid 50 EC, Feniton 50 EC
39 Malathion Limithion 57 EC, Razthion 57 EC
40 Phenthoate Cidial 50L, Cidial 5G
41 Fipronil Goolee 50 SC
42 Imidaclorpid Admire 200 SL, Tiddo 200 SL, Confidor 70
WG, Impale 20 SL
43 Thimethoxam Actara 25 WG, Cruizer 70 WS
44 Pirimiphos methyl Silosan 50 EC, Super Guard 50 EC
45 Glyphosate Touchdown, Sun Up, Touchdown HiTech
500 SL
46 2,4-D Fielder, 2,4-D Amine
47 Paraquat Gramoxne, Paraxone
48 Oxadiazon Ronstar 25 EC
49 Oxadiarzyl Topstar 400 SC
50 Glufosinate-ammonium Basta 15 SL
51 Anilofos Basta 15 SL
52 Butachlor Aimchlor 5 G, Nuchlor 5 G
53 Pretilachlor Rifit 500 EC, Superheat 500 EC, Prechlor
500 EC
54 Ethoxysulfuran Sunrice 150 WG
55 Triosulfurn+Dicamba Lintur 70 WG
56 Metribujin Sencor 70 WP
37
57 S-metolachlor Dual Gold 960 EC
58 Orthosulfamuron Kelion 50 WP
59 S.Bioallerthrin+Permethrin ACI Aerosol Insect Spray
60 Deltamethrin Delete 2.5 EC, Sislin 2.5 EC, Crackdown,
K-Orthrin 1% SC, K-Orthrin 5% WP
61 Permethrin Coopex 25 WP
62 Chlorpyriphos Aciphos 20 EC
63 Pirimiphos methyl Actelic 50 EC, Cleaner 50 EC
64 Temephos Missile 50 EC
65 Phenthoate Noback 50 L
66 Cypermenhrin Demon 10 EC, Keeper 10 EC
67 Lambda Cyhalothrin Shooter 2.5 EC
68 S.bioallethrin+Permathrin+Piperanyl
Resigen OS
Butoxide
69 S-Bioallethrin Xpel Super Mosquito Coil
70 ETOC & Sumithrin (d-Phenothin) Xpel Aerosol,
71 ETOC & Sumithrin New ACI Aerosol Insect Spray
72 Permethrin, Tetramethrin, Es
ACI Liquid Insecticide
bioalletthrin
73 d-teramethrin+Permethrin Globe Aerosol
74 Metofluthrin 0.005% ACI Mosquito Coil Super, ACI Mosquito
Coil Super Plus
75 Imiprothrin+Deltamethrin ACI Cockroach Spray
76 Prallethrin Mortien Deep Reach Liquid M.Coil
01712590747 Monirul Islam Chif Eng.
Further Reading:
1.
www. picbd.org
2.
www.toxinz.com
3.
www.wikietox.com
4.
www.toxinology.com
5.
www.who ipcs.com
6.
www.sacatrac.org
7.
www.apamt.com
38

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Contents

Management of Poisoning Guideline-

National Poison Information Centre

Dhaka Medical College

World Health Organization (WHO)

Training Manual on Management of Poisoning

Prof. Md. Abul Faiz

Dr. Shakil Ahmed

Dr. Md. Robed Amin

Dr. Aniruddha Ghose

Dr. Md. Mizanul Hoque

National Poison Information Centre

Dhaka Medical College

World Health Organization (WHO)

STATEMENT OF WHO ENVIRONMENTAL HEALTH UNIT

promotion, through the Department of Public Health Engineering.

implementation of water safety plans, which is fundamental to a preventive water management

partners to remedy this situation.

Access to adequate sanitation has been dramatically increased as a consequence of the

coverage by 2010. In addition to the necessary infrastructure attention must be given to

promotion should continue to be pursued.

associated with environmental pollution or degradation. These programmes are undertaken in

capacity building of sanitary inspectors at the Upazilla level.

Environmental Health Unit

world Health Organization

DPHE Bhaban (4th floor)

14, Shaheed Cap. MonsurAli Sarani Kakrail,

Dhaka 1000, Bangladesh

TRAINING MANUAL ON MANAGEMENT OF POISONING

First Published- November 2007, Dhaka, Bangladesh.

Environmental Health Unit

All rights reserved by -

Environmental Health Unit

ISBN: 984 300 00062 6

Guideline updated: 2009 by

National Poison Information Centre

Dhaka Medical College

World Health Organization (WHO)

organism, causes injury or death.”

deforestation, rapid urbanization and industrialization, which in turn produce environmental

are accidental poisoning cases.

updated knowledge base skills.

readers will further furnish this book and are welcome.

1. Prof. Md. Abul Faiz Chairman

Professor of Medicine Module Committee

Dhaka Medical College. PlC, DMCH.

2. Prof. Md. Akhtaruzzaman (Late) Member

Ex-Professor and Head of the Dept. of

Professor & Head of the Dept. of Forensic Medicine

Professor & Head of the Dept. of Paediatrics

LIST OF RESOURCE PERSONS in 1st edition

(Participated in workshop for finalization

of the draft module on 30/05/07 held in Dhaka Medical College)

1. Dr. Md. Shahjahan Bishwas Director General of Health Services, GOB

2. Brig. General Sarker M A Matin Director, Dhaka Medical College Hospital

3. Prof. Md. Abul Faiz Principal, Dhaka Medical College

4. Prof. Md. Shahadat Hossain Dhaka Medical College

5. Dr. Andrew Trevett WHO EH Advisor, Bangladesh

6. Prof. M A Kasham Khandaker Dhaka Medical College

7. Prof. Abu Azahar Sir Salimullah Medical College

8. Prof. FM Siddiqui Dhaka Medical College

9. Prof. Md. Shah Alam Faridpur Medical College

10. Prof. Kazi Md. Jahangir Rangpur Medical College